pass program

Course Instructors: Dr. Francis, Dr. Wolf and Dr. Bautista

Hemostasis

Lymphoma & Leukemia

251

Amino Acids

Biochemistry

Endocrinology

Neurophysiology

Hematology

Vitamins, Minerals, Trace Elements

Cellular Physiology

Membrane Physiology

244

Low Energy State

Inflamation

Nephritic-Nephrotic

254

248

218

Reproductive Endocrinology

Renal Physiology

76

159

171

192

220

Gastrointestinal Physiology (GI) 135

545

53

55

80

87

64

71

105

116

125

Electrolyte Physiology

Pulmonary Physiology

Neuromuscular Physiology

Vascular Physiology

Cardiac Physiology

PageLecture

Note Pages

Welcome to the Program

Rheumatology

238

PASS PROGRAMUSMLE REVIEW STEPS 1, 2 AND 3

Course Instructors: Dr. Francis, Dr. Wolfe & Dr. Bautista

184

1

Anabolic Pathways

Cancers

Immunodeficiencies

Lymphocytes

Leukocytes

Immunology

Catabolic Pathways

Protein Structure and Function

Enzymes

MicrobiologyAntibiotics

Granulocytes

Biochemistry, Glycolysis, Gluconeogenesis & TCA

Viruses

497

515

Antibiotics (Dr. Cordova)Surgery & Trauma (Dr. Cordova)

413453477

408

292

303

329

335

344

371

262

277

282

351

358

369

Obstectrics and GynecologyNote Pages

The Four Hypersensitivities 366

2

4/30/2008

1

Making the most out of your time here at the PASS

program !!!

Making the most out of your time here at the PASS

program !!!

Study smart not hard

Study smart not hard

Power is in knowledge !Power is in knowledge !gg

NBME- National Board of Medical ExaminersNBME- National Board of Medical Examiners

ForFor profit company NBME- National Board

of Medical ExaminersNBME- National Board of Medical Examiners

Shortage of family doctors throughout US

Shortage of OB/GYN physicians in Fl,

Shortage of family doctors throughout US

Shortage of OB/GYN physicians in Fl, p yTexas, California, and Michigan

Cutoff for USMLE Steps were raised from 182 to 185?

p yTexas, California, and Michigan

Cutoff for USMLE Steps were raised from 182 to 185?

Youre the next cutting edge physician

20,000 new residents Your pay?

Youre the next cutting edge physician

20,000 new residents Your pay?

What do you want to do when you finish medical school?

What do you want to do when you finish medical school?

p y Radiology, Dermatology,

Ortho.

Those making decisions, control how many come across the bridge

p y Radiology, Dermatology,

Ortho.

Those making decisions, control how many come across the bridge

45

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2

Why do so many fail the test?

Why do so many fail the test?ZOO

THEORYTHEORY

A physician sits and writes a question based off of the discipline they want to test you on

A h l i t d th ti th

A physician sits and writes a question based off of the discipline they want to test you on

A h l i t d th ti th

How do they comprise a test that is written for you to fail?How do they comprise a test

that is written for you to fail?

A psychologists rewords the question the way your mind thinks This is why the wrong answers always look good

A psychologists rewords the question the way your mind thinks This is why the wrong answers always look good

5 PASS rules in answering question


1. Cover the answers 2. Read the last sentence and decide if it is a clue or concept

1. Cover the answers 2. Read the last sentence and decide if it is a clue or concept



1. Cover the answers 2. Read the last sentence and decide if it is

a clue or concept question

1. Cover the answers 2. Read the last sentence and decide if it is

a clue or concept questionit is a clue or concept question

3. Read the vignette, and isolate the facts of the vignette

4. Comprise a thought process 5. Look down, click and move !!!!!!!

it is a clue or concept question







A 38 y/o woman has congestive heart failure,premature ventricular contractions and

repeated episodes of ventricular tachycardia.Her blood pressure is normal and there are nomurmurs. Her heart is markedly enlarged.

A 38 y/o woman has congestive heart failure,premature ventricular contractions and

repeated episodes of ventricular tachycardia.Her blood pressure is normal and there are nomurmurs. Her heart is markedly enlarged.

Coronary angiography shows no abnormalities.

Which of the following is the most likely diagnosis ?

Coronary angiography shows no abnormalities.

Which of the following is the most likely diagnosis ?

A.Acute rheumatic feverB.Congenital fibroelastosisC.Constrictive pericarditisD.Myocardial infarction

A.Acute rheumatic feverB.Congenital fibroelastosisC.Constrictive pericarditisD.Myocardial infarctionE.Primary cardiomyopathyE.Primary cardiomyopathy

A.Acute rheumatic feverB.Congenital fibroelastosisC.Constrictive pericarditisD.Myocardial infarction

A.Acute rheumatic feverB.Congenital fibroelastosisC.Constrictive pericarditisD.Myocardial infarctionE.Primary cardiomyopathyE.Primary cardiomyopathy

46

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3

USMLE Step 2 and Step 3 approachUSMLE Step 2 and Step 3 approachWhat is the next best step in management?

Is the patient stable? (based on hemodynamics)- Unstable: ABCs- Stable: read the vignette

What is the next best step in management?

Is the patient stable? (based on hemodynamics)- Unstable: ABCs- Stable: read the vignette

Do you have enough information to make a definitive diagnosis?- Yes- treat- No- order a test (BLIS) blood/labs/image/surgery

Do you have enough information to make a definitive diagnosis?- Yes- treat- No- order a test (BLIS) blood/labs/image/surgery

A 23 y/o man who is HIV positive has a 2 weekhistory of midsternal chest pain that is aggravatedby eating spicy foods; the pain is unrelated toexertion or position and he reports no dysphagia.Treatment with H2 receptor blocking agents hasprovided no relief. He takes clotrimazole forthrush and zidovudine (AZT). He has a CD4+ T

A 23 y/o man who is HIV positive has a 2 weekhistory of midsternal chest pain that is aggravatedby eating spicy foods; the pain is unrelated toexertion or position and he reports no dysphagia.Treatment with H2 receptor blocking agents hasprovided no relief. He takes clotrimazole forthrush and zidovudine (AZT). He has a CD4+ T( )lymphocyte count of 220/mm3 (N>500).

Which of the following is the most appropriate next step in management?

( )lymphocyte count of 220/mm3 (N>500).

Which of the following is the most appropriate next step in management?

A.Therapeutic trial of acyclovirB.24 Hour pH probeC.Acid perfusion testD.Esophageal manometry

A.Therapeutic trial of acyclovirB.24 Hour pH probeC.Acid perfusion testD.Esophageal manometryE.EsophagoscopyE.Esophagoscopy

A.Therapeutic trial of acyclovirB.24 Hour pH probeC.Acid perfusion testD.Esophageal manometry

A.Therapeutic trial of acyclovirB.24 Hour pH probeC.Acid perfusion testD.Esophageal manometryE.EsophagoscopyE.Esophagoscopy

Procrastination in doing questions


How many read before doing questions?Wh t t ti ?

How many read before doing questions?Wh t t ti ?What are you testing ?2 weeks later, what happens?

What are you testing ?2 weeks later, what happens?

Procrastination in doing questionsProcrastination in doing questions

How many read all the choices in the explanation?

f

How many read all the choices in the explanation?

fPrior exposure to future questions

I have a lot of details in my head

Prior exposure to future questions

I have a lot of details in my head

47

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4



How many do the questions in tutor mode?

How many do the questions in tutor mode?

Driving a car and lost

Driving a car and lost

Its ok to be wrong !!!!Its ok to be wrong !!!! Block of 50 question and get

45/50 correct, are you any more prepared for the boards from the moment you started that test?

Block of 50 question and get 45/50 correct, are you any more prepared for the boards from the moment you started that test?

If you get 30 /50 wrong, you will not be very happy

Found a hole, that can be fixed

Remember every time you fall

If you get 30 /50 wrong, you will not be very happy

Found a hole, that can be fixed

Remember every time you fall

Why do we not listen to our first thought?

Why do we not listen to our first thought?

We are scared of being wrong We are scared of being wrong

We do not want our over all average to be lower than the mean

We do not want our over all average to be lower than the mean

My friends told me to do as many questions as I can before I take the test

My friends told me to do as many questions as I can before I take the test

6000 questions Multiple banks You are doing questions to learn

from them Do we order test to learn about a

pathology (i.e. Hypothyroidism TSH panel)

6000 questions Multiple banks You are doing questions to learn

from them Do we order test to learn about a

pathology (i.e. Hypothyroidism TSH panel)

3 steps to studying:1. Obtain the information2. Questions3. Results of the bank

3 steps to studying:1. Obtain the information2. Questions3. Results of the bank

Questions: Organ system based 50 question

Questions: Organ system based 50 question

Do they ask you 50 new things?

Pathological presentation does not change, just the story line (clues are so important)

Will you see the pattern in mixed blocks?

Do they ask you 50 new things?

Pathological presentation does not change, just the story line (clues are so important)

Will you see the pattern in mixed blocks?

What bank to use?What bank to use?Q-Bank USMLE Rx. USMLEworldQ-Bank USMLE Rx. USMLEworld

Do you see a pattern?

At the end of your first week, you will be evaluated by several tutors to determine which is the best test bank for you to use.

Do you see a pattern?

At the end of your first week, you will be evaluated by several tutors to determine which is the best test bank for you to use.

48

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5

What should I do, with the results of my question bank?What should I do, with the results of my question bank?

50 questions completed (what is right or wrong)

Example: Polyhydramnios: Down syndrome

50 questions completed (what is right or wrong)

Example: Polyhydramnios: Down syndromeExample: Polyhydramnios: Down syndrome What is the most common cardiac

abnormality?

Write the subject matter Look for patterns in the question This is what you will read about

Example: Polyhydramnios: Down syndrome What is the most common cardiac

abnormality?

Write the subject matter Look for patterns in the question This is what you will read about

What do most students doWhat do most students do Vignette.. Downs syndrome

Answer: Endocardial cushion defect

Read about it from the author Transcribe to note cards on ECD

Vignette.. Downs syndrome Answer: Endocardial cushion defect

Read about it from the author Transcribe to note cards on ECDTranscribe to note cards on ECD Read the notes about ECD Read the CMDT about ECD Harrisons and read about ECD

Are you any more prepared for Downs syndrome on the boards?

Transcribe to note cards on ECD Read the notes about ECD Read the CMDT about ECD Harrisons and read about ECD

Are you any more prepared for Downs syndrome on the boards?

NBME practice examNBME practice exam

On line at http://www.NBME.org Step 1 5 forms (do not take form 3) Step 2 3 forms

On line at http://www.NBME.org Step 1 5 forms (do not take form 3) Step 2 3 forms Step 3 1 form

When should I take may NBME ?

Step 3 1 form

When should I take may NBME ?

Not enough time in the day !!!!!!!- Exercise- 210 score- Proper sleep hygiene- Proper sleep hygiene-Take time out to

reward yourself

PASS program clues vs. class notesPASS program clues vs. class notes

You should drill the PP-clues with a partner for at least 1 hour a night. ( hour new, hour random review)

You should drill the PP-clues with a partner for at least 1 hour a night. ( hour new, hour random review)

Caution in drilling class notes: Teacher vs. Student

Caution in drilling class notes: Teacher vs. Student

Tutoring:Tutoring: This is your time to ask questions that

you may have with the material

Do questions with your tutor (remember

This is your time to ask questions that you may have with the material

Do questions with your tutor (rememberDo questions with your tutor (remember its ok to be wrong)

Your tutor is there to help you find and fix your weakness

Do questions with your tutor (remember its ok to be wrong)

Your tutor is there to help you find and fix your weakness

49

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6

Tutoring cont.Tutoring cont. Try several tutors to find the chemistry that

works for you

If you can not make it to your secession, please inform your tutor, so they can fill the spot with another student

Try several tutors to find the chemistry that works for you

If you can not make it to your secession, please inform your tutor, so they can fill the spot with another student

Once you are comfortable with a couple of tutors, there is a request book in the back.

(The key word, just a request book)

Once you are comfortable with a couple of tutors, there is a request book in the back.

(The key word, just a request book)

50

Physiology: Weeks One & Two

5151

1INTRODUCTION: THE MOST POWERFUL CONCEPT IN

MEDICINE

THE LOW ENERGY STATE

WHO USES ENERGY? BRAIN MUSCLES PRIMARY ACTIVE TRANSPORT HEART MEMBRANE MOVEMENT

RAPIDLY DIVIDING CELLS SKIN HAIR GI RESPIRATORY RENAL(PCT) BLADDER ENDOMETRIUM ENDOTHELIUM BREASTS SPERM GERM CELLS CUTICLES BONE MARROW

RED BLOOD CELLS WHITE BLOOD CELLS PLATELETS

PRESENTATION OF A DISEASE When it bothers the patient enough, he or

she will see the doctor as soon as possible Weakness so that the patient can not go to

work Shortness of breath scares people; they think

they might die

SIGNS OF DISEASE: WHAT YOU CAN SEE

TACHYPNEA and DYSPNEA

SYMPTOMS: THE PATIENTS COMPLAINTS

WEAKNESS SHORTNESS OF BREATH

MOST COMMON INFECTIONS PULMONARY INFECTIONS URINARY TRACT INFECTIONS

5353

2OTHER COMPLICATIONS Dry skin Hair dry and brittle Nails brittle Bone marrow suppressed

Anemia Leukopenia Thrombocytopenia

COMPLICATIONS, cont Endothelium atrophic Endometrium

atrophic Breasts atrophic Sperm count low GI nausea, vomiting

and diarrhea Renal- PCT shuts

down

Bladder atrophic; leads to UTIs

Respiratory weak cough > infections

Germ cells unable to replicate > leads to skin and GI cancers

CNS: MR (children) and dementia (adults)

CV heart failure

MOST COMMON CAUSE OF DEATH?

HEART FAILURE!!!

ANYTIME YOU CAN CONNECT TO THE LOW ENERGY STATE

APPLY THE ENTIRE CONCEPT THIS ACCOUNTS FOR

APPROXIMATELY 98% OF ILLNESSES WHENEVER IN DOUBT > ASSUME IT IS

A LOW ENERGY STATE

STOP GUESSING!!!

5454

VITAMINS, MINERALS andTRACE ELEMENTS

THE BEGINNING

Vitamin A A cofactor for PTH Necessary for CSF production Used for epithelial maturation, especially

hair, skin, and eyes Most unique function is night vision A mild antioxidant

Vitamin A deficiency

Poor night vision Decreased CSF production: asymptomatic Hypoparathyroidism Epithelial cells fail to mature

Vitamin A excess

Pseudotumor cerebri: excess CSF production

Hyperparathyroidism: moans, groans,bones and stones

Pseudotumor Cerebri

Sign: papilledema Symptom: headache Evaluation: CT scan ( shows enlarged

ventricles) Treatment: d/c vitamin A; serial LPs (30cc at a

time) Main complication: blindness This is the only cause of increased ICP where

you dont have to worry about herniation

Vitamin B1: Thiamine Necessary for four important enzymes:

Pyruvate dehydrogenase Alpha-ketogluterate dehydrogenase Branched chain amino acid dehydrogenase Transketolase

5555

Thiamine Deficiency Beriberi

Dry beriberi Wet beriberi

Wernickes Encephalopathy Receptive aphasia

Wernicke-Korsakoff syndrome Mamillary bodies now also involved Confabulation Inability to move short-term memory to long-term

memory

Vitamin B2: Riboflavin Used in cofactors ( FAD) Best source is milk Sunlight breaks riboflavin down

Riboflavin deficiency

Angular Cheilosis

Vitamin B3: Niacin Necessary for cofactors ( NAD, NADH,

NADP, NADPH) Needed by pyruvate dehydrogenase,

alpha-ketogluterate dehydrogenase, and branched chain amino acid dehydrogenase

Niacin deficiency

Pallegra : 4 Ds diarrhea, dermatitis, dimentia and death

Hatnups disease: presents just like pallegra Defective renal transport of tryptophan

Vitamin B4: Lipoic acid Needed by pyruvate dehydrogenase,

alpha-ketogluterate dehydrogenase, and branched chain amino acid dehydrogenase

No deficiency state

5656

Vitamin B5: Panthotenic Acid Needed by pyruvate dehydrogenase,

dehydrogenase, alpha-ketogluterate dehydrogenase, and branched chain amino acid dehydrogenase

No deficiency state

Vitamin B6: Pyridoxine Needed by all transaminases INH pulls pyridoxine out of the body Forms the cofactor pyridoxalphosphate

Pyridoxine deficiency

neuropathy

Vitamin B9: Folate The first vitamin to run out whenever you

have rapidly dividing cells Used to make tetrahydrofolate (THF) from

which you make nucleotides

Folate deficiency

Megaloblastic anemia Hypersegmented neutrophils Neural tube defects in fetuses Mcc: overcooked vegetables

Vitamin B12: Cyanocobalamin Needed by two enzymes:

Homocysteine methyltransferase Methylmalonyl-CoA mutase

Used to make tetrahydrofolate Used to recycle odd-numbered carbon

fatty acids

5757

Vitamin B12 deficiency

Megaloblastic anemia Hypersegmented neutrophils Neuropathy, especially involving the dorsal

column pathways and corticospinal tracts Mcc: pernicious anemia (type A gastritis)

Vitamin C Used for hydroxylation Hydroxylates proline and lysine in collagen

and elastin Main antioxidant in the GI system

Vitamin C deficiency

Scurvy Bleeding from hair follicles and gums

Vitamin D Necessary for bone and teeth formation Stimulates osteoblastic activity Stimulates calcium AND phosphorous

absorption and reabsorption Mineralizes bones and teeth

Vitamin D deficiency

Rickets: in children Lateral bowing of the legs Osteomalacia: in adults

Vitamin D resistant rickets Defective renal reabsorption of phosphorous As phosphorous leaks out, it pulls calcium

with it

Vitamin E The main antioxidant in your blood Absorbs free radicals

5858

Diseases involving oxidation

Cancer Alzheimers disease Coronary artery disease Hemolytic anemia ( esp. G6PD)

Antioxidants

Vitamin E: in blood Vitamin C: in GI tract Vitamin A Beta-Carotene

Biotin

Necessary for carboxylation

Biotin deficiency

Many carboxylases would lose their function

Vitamin K Needed for gamma-carboxylation Adds a third (gamma) carboxyl group to

the vitamin k dependent clotting factors Clotting factors II, VII, IX, X, Protein C &

Protein S Protein C has shortest half life, followed by

factor VII

Warfarin

Competitive inhibitor of vitamin K Given orally Always give heparin first Crosses the placenta Teratogenic Follow PT ( prothrombin time ) INR 2 to 3x normal

5959

Heparin

Acts as a cofactor for antithrombin III Blocks thrombin, as well as clotting factors

IX, X, XI, and XII Follow by measuring PTT ( INR 2 3X NL) To reverse the action: protamine sulphate If patient acutely bleeding: give FFP to

reverse immediately

What are germs good for?

Vitamins related to gut flora

They make: 90% of vitamin K Biotin Folate Panthotenic acid

They help absorb Vitamin B12

MINERALS

Minerals

Calcium Magnesium Zinc Copper Iron

Calcium Intracellular calcium needed for all muscle

contraction Smooth muscle uses extracellular calcium

for second messenger systems Atrium is ONLY membrane that uses

calcium to depolarize Cardiac ventricle depends on extracellular

calcium to trigger off its intracellular calcium release

6060

Calcium, cont

Used for axonal transport Presynaptic influx of calcium necessary for

release of ALL neurotransmitters Needed for normal bone and teeth

development

Magnesium A cofactor for ALL kinases A cofactor for PTH Interacts with potassium as well, but

location currently unknown

Zinc Needed by hair, skin, sperm and taste

buds

Zinc deficiency: dysguisia

Copper Needed by lysine hydroxylase in the

formation of collagen Also needed by complex IV of electron

transport system

Copper excess

Wilsons disease Autosomal recessive Ceruloplasmin deficiency Copper deposition in lenticular nucleus (basal

ganglia), iris (Kayser-Fleischer rings) and in the liver (causing cirrhosis)

Tx: penicillamine

Movement disorder in a middle-aged person

HUNTINGTONS DISEASE (90%) Autosomal dominant Trinucleotide repeats Involves caudate

nucleus Has anticipation Treat with

antipsychotics Mcc of death: suicide

WILSONS DISEASE Autosomal recessive Ceruloplasmin def Copper deposition in

lenticular nucleus, liver and iris

Treat: penicillamine

6161

Trinucleotide repeats Huntingtons disease Fragile X Fredriecks ataxia Prader Willi syndrome Myotonic dystrophy

Iron Needed for formation of heme and

hemoglobin Ferrous iron binds oxygen Needed by complex III and IV of electron

transport system

And finally the trace elements Trace Elements

Chromium Selenium Molebdenum Manganese Tin Flouride

Chromium Enhances insulin action Def: causes diabetes

Selenium Needed primarily by the heart Excess: breath smells like garlic ( arsenic

as well) Def: dilated cardiomyopathy

6262

Molebdenum and Manganese Needed by many enzymes in glycolysis Xanthine oxidase: needs both elements

Tin Needed for hair growth

Flouride Needed for teeth and bone growth Excess: blocks enolase of glycolysis THE END

BUT, it is really the beginning

6363

CELLULAR PHYSIOLOGY CELL ORGANELLS

IRREVERSIBLE CELLULAR INJURY APOPTOSIS

CELL MEMBRANE DISSOLVES FIRST

PROGRAMMED CELL DEATH

NONINFLAMMATORY

PYKNOSIS KARYORHEXXIS KARYOLYSIS

NECROSIS NUCLEUS

DISSOLVES FIRST UNEXPECTED INVOLVES

INFLAMMATION

PYKNOSIS KARYORHEXXIS KARYOLYSIS

NECROSIS ISCHEMIC(COAGULATIVE) PURULENT GRANULOMATOUS FIBRINOUS CASEOUS FAT HEMORRHAGIC LIQUEFACTIVE



6464






MESS WITH THE CHROMOSOMES

MONOSOMIES: DIE! DIE! DIE! MCC: NONDISJUNCTION

90% IN DAD, USUALLY IN MEIOSIS 1; BUT SPERM DIE ON A DAILY BASIS

FEWER OCCUR IN MOM; BUT MOM KEEPS HER EGGS FOR LIFE AND IS THEREFORE MORE LIKELY TO TRANSMIT HERS

IF ONE WERE TO SURVIVE TO BE BORN, IN THE LEAST, THINGS WILL NOT GROW

6565

TURNER SYNDROME WEBBED NECK CYSTIC HYGROMA GONADAL STREAKS SHIELD-SHAPED CHEST COARCTATION OF AORTA

TRISOMIES DIE! DIE! FEW LIVE TRISOMIE 13: PATAU SYNDROME

POLYDACTYLY PALATE IS HIGH-ARCHED PEE-ING SYSTEM ABNORMALITY

TRISOMIES TRISOMIE 18: EDWARDS SYNDROME

ROCKERBOTTOM FEET (IN 95%)

TRISOMIES TRISOMIE 21: DOWNS SYNDROME

MCC: NONDISJUNCTION ROBERTSONIAN TRANSLOCATION:

HIGHEST INCIDENCE (33% OF OFFSPRING)

HAS MANY THINGS TO CONSIDER

DOWNS SYNDROME

MENTAL RETARDATION 100% IQ: AVERAGE IS 85 TO 100 WITH A STANDARD

DEVIATION OF 15 SUPERIOR INTELLIGENCE: IQ > 130 MILD MR: IQ < 70 MODERATE MR: IQ < 55 SEVERE MR: IQ < 40 PROFOUND MR: IQ < 25 NEEDS 24HR CARE MILD TO MODERATE MR CAN BE TAUGHT BASIC

ADLS

6666

DOWNS SYNDROME

EARLY-ONSET ALZHEIMER DISEASE HIGHER FREQUENCY OF AML;BUT ALL IS THE

MOST COMMON LEUKEMIA

20 TO 40% HAVE congenital heartDISEASE

-ENDOCARDIAL CUSHION DEFECTS VSD and ASD VSD ASD

DOWNS SYNDROME

CYANOTIC CONGENITAL HEART DISEASE TRANSPOSITION OF GREAT ARTERIES TETROLOGY OF FALOT

DOWNS SYNDROME

50% HAVE HYPOTHYROIDISM WIDELY-PACED CRANIAL SUTURES MACROGLOSSIA DUODENAL ATRESIA HIRSCHSPRUNGS DISEASE CLUES:

MONGLIAN SLANT TO EYES WIDELY SPACED FIRST AND SECOND TOES SIMIAN CREASE

TRISOMIES

XXX: Normal female; has two barr bodies XXY: Klinefelters syndrome. Tall male

with gynecomastia, small penis and testicles

X- Fragile X syndrome Mcc of chromosomal induced MR Short stature; macrochordism Collagen disorder (increased risk of MVP) Isolated using the drug METHOTREXATE

Chemotherapy

6767

Josh

Josh

Josh

Josh

Josh

Josh

Josh

Josh

Josh

Josh

Josh

Josh

Josh

CHEMOTHERAPY

Stops rapidly dividing cells Attacks the nucleus in some way Causes irreversible cellular death WILL kill some patients No such thing as safe chemo

ANTIMETABOLITES ARA-A ARA-C 5-FU: blocks thymidylate synthetase 6-MERCAPTOPURINE: promotes gout; recognized by

xanthine oxidase THIOGUANINE METHOTREXATE: inhibits dihydrofolate reductase(as

does TRIMETHOPRIM and PYREMETHAMINE) Most commonly used antimetabolite Used to treat molar pregnancies Used to treat STEROID RESISTANT disease( followed by

AZOTHIOPRINE and CYCLOSPORINE)

ANTIMETABOLITES METHOTREXATE

Causes folate deficiency and megaloblastic anemia

Give LEUCOVORIN > FOLINIC ACID to prevent the anemia

ANTIMETABOLITES AZOTHIOPRINE

Used for steroid resistant diseases( behind METHOTREXATE and before CYCLOSPORINE)

ALKYLATING AGENTS Bind to double stranded DNA Used primarily for slow growing cancers Cause the most nausea and vomiting

ONDANSETRON: serotonin blocker used to treat nausea and vomiting in chemotherapy

ALKYLATING AGENTS Bleomycin Busulphan Adriamycin Cisplatnin Cyclophosphamide Isophosphamide Mitomycin Antimycin Acridine dyes

Hydroxyurea Melphalan Mechlorethamine Procarbazine Dacarbazine Chlorambucil

FOR RESCUES Desroxzasane Mesna

6868

MICROTUBULE INHIBITORS Vinblastine Vincristine Paclitaxel

NUTRIENT DEPLETION L-ASPARAGINASE

IMMUNEMODULATORS LEVAMISOLE

IRREVERSIBLE CELLULAR DEATH

NUCLEAR DAMAGE LYSOSOMAL DAMAGE MITOCHONDRIAL DAMAGE

OCCURS IN 6 HOURS in all tissues

6969


NUCLEAR DAMAGE LYSOSOMAL DAMAGE MITOCHONDRIAL DAMAGE

OCCURS IN 6 HOURS in all tissues except the brain


OCCURS IN 20 MINUTES IN THE BRAIN

The End?To Be Continued

7070

MEMBRANE PHYSIOLOGY

A MEMBRANES JOB IS NEVER DONE

WHAT A MEMBRANE DOES

PROVIDE SHAPE AMPHIPATHIC

HYDROPHILIC and HYDROPHOBIC WATER SOLUBLE and FAT SOLUBLE HYDROPHOBIC wants to be INSIDE away from

water HYDROPHILIC wants to be OUTSIDE in contact

with water

FAT SOLUBLE COMPOUNDS DO NOT interact with the outer cell

membrane. They go right through and head for the nucleus

HAVE NUCLEAR MEMBRANE RECEPTORS

Concentration gradient is only limiting factor

STEROID HORMONES MADE FROM CHOLESTEROL FAT SOLUBLE( hydrophobic) Do NOT interact with cell membrane ALL have a nuclear membrane receptor

except CORTISOL CORTISOL has a cytoplasmic receptor;

but it still translocates to the nuclear membrane

7171

WATER SOLUBLE HORMONES HYDROPHILIC CAN NOT simply go through a fat soluble

membrane Must bind to the outside membrane to a

receptor Requires a SECOND MESSENGER But first, what about ANY water soluble

compound?

WATER SOLUBLE COMPOUNDS Factors affecting diffusion

CONCENTRATION GRADIENT SIZE of molecule Net charge on molecule pH (affects the net charge of a molecule) THICKNESS of membrane SURFACE AREA of membrane FLUX (dx/dt) REFLECTION COEFFICIENT

NUMBER OF PARTICLES RETURNED / NUMBER OF PARTICLES SENT TO MEMBRANE

FICKS EQUATION Factors that FAVOR diffusion go in the

NUMERATOR Factors that NEGATIVELY affect diffusion

go in the DENOMINATOR

OTHER FUNCTIONS OF A MEMBRANE

CREATE and MAINTAIN concentration gradients

SELECTIVE permeability Has SATURATED fats( no double bonds) Has UNSATURATED fats( double bonds)

Easier to break down Better temperature regulation More fluidity of movement, especially lateral

ESSENTIAL FATS Can get them ONLY through the diet LINOLENIC LINOLEIC

Used to make ARACHADONIC ACID Arachadonic acid becomes essential if linoleic

acid is missing from the diet

OTHER MEMBRANE FUNCTIONS PHAGOCYTOSIS: requires energy

ENDOCYTOSIS: primarily for nutrition EXOCYTOSIS: primarily for getting rid of

waste products ( i.e. lipofuscin ) PINOCYTOSIS: for movement of fluids and

electrolytes SKIN is only organ that does this process

7272

OTHER MEMBRANE FUNCTIONS TEMPERATURE REGULATION

RADIATION > concentration gradient CONDUCTION > requires contact CONVECTION > movement of environment

drags heat out of the body

OTHER MEMBRANE FUNCTIONS ALL membranes can depolarize Resting membrane potentials

ELECTROLYTE MOVEMENT CONCENTRATION GRADIENT ELECTRICAL GRADIENT DRIVING FORCE NERNST NUMBER (E-ion) CONDUCTANCE (G-ion) PERMEABILITY

CHANNELS: small ions PORES: medium-sized molecules (sweat) TRANSPORT PROTEINS

TRANSPORT PROTEINS PRIMARY ACTIVE TRANSPORT

>requires an ATPase. Going against a gradient

SECONDARY ACTIVE TRANSPORT Requires sodiums gradient SYNPORT or COTRANSPORT >moving in

the same direction as sodium ANTIPORT > movement in opposite direction

as sodium

SECOND MESSENGERS C-amp > most common second messenger

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PHOSPHODIESTERASE INHIBITORS CAFFIENE THEOPHYLLINE

SILDENAFIL VARDENAFIL TADALAFIL

SECOND MESSENGERS, cont IP3 -DAG

IP3-DAG SYSTEM All HYPOTHALAMIC HORMONES, except

CRH All SMOOOTH MUSCLE CONTRACTION

by hormone or neurotransmitter

CALCIUM CALMODULIN SYSTEM 4 calcium molecules: 1 calmodulin All SMOOTH MUSCLE CONTRACTION

by DISTENTION

CALCIUM Used as a second messenger by

GASTRIN only

TYROSINE KINASE INSULIN and all GROWTH FACTORS

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NITRIC OXIDE NITRIC OXIDE > GUANYLATE CYCLASE

> elevates c-GMP

NITRATES ENDOTOXIN ANP

NITRATES VASODILATORS TACHYPHYLAXIS; rapid tolerance

Nitroglycerin Dinilatrate Sodium Nitroprusside

The End

Insane in the membrane

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INFLAMMATION SHUTTING DOWN THE Na-K ATPase Potassium still leaks out Cell becomes more negative > less likely

to depolarize

SHUTTING DOWN THE Na-K ATPase, cont

With Na trapped within the cell, calcium also gets trapped within the cell This increases contractility

DIGITALIS DIGITOXIN OUBAIN

EKG CHANGES Na-K ATPase shuts down when a vessel

is 70% stenosed Potassium leaks out, making cells more

negative This is why you get ST-wave

DEPRESSION

ST-WAVE DEPRESSION Early ischemia 70% stenosis SYMPTOMS BEGIN Subendocardial ischemia STABLE ANGINA

Comes on with exertion; goes away with rest 30% flow is enough at rest, but not on exertion TX: VASODILATORS > increase radius increases

flow

FOLLOW-UP FOR ANGINA PAIN GOES AWAY

Hospitalize for 24hours Do serial EKGs and CIEs (Q6h x 24h) If negative workup, then discharge home Do a regular STRESS TEST in 6 weeks Do STRESS THALLIUM test in 6 weeks

Thallium flows through the coronary arteries Look for COLD AREAS: NO FLOW( ISCHEMIC)

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FOLLOW-UP FOR ANGINA, cont If you think they might have had an MI,

then do a Ca-PYROPHOSPHATE scan Cells that die calcify Dead cells will take up the Ca-

PYROPHOSPHATE Look for a HOT SPOT

FOLLOW-UP FOR ANGINA, cont IF PATIENT UNABLE TO PERFORM THE

STRESS TEST: DOBUTAMINE STRESS TEST DIPYRIDAMOLE STRESS TEST

EKG CHANGES

Na gets trapped within a cell when there is at least 90% stenosis

Cells become more POSITIVE

UNSTABLE ANGINA 90% stenosis EVENTS OCCUR PLAQUE RUPTURED, and platelets are

closing off the rest of the lumen TX: Aspirin > Nitrates> Oxygen > Heparin

> tPa > Morphine > B-blockers > Take to CATH LAB for angiogram

ANGIOGRAM FINDINGS LEFT MAIN CORONARY ARTERY

OCCLUSION ( 70% stenosis or more) THREE OR MORE VESSELL DISEASE

TX: GO STRAIGHT TO SURGERY

ANGIOGRAM FINDINGS, cont ANY SINGLE OR DOUBLE VESSELL

DISEASE

TX: PTCA with STENT placement coated with CLOPIDOGREL

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CELLS ARE MORE LIKELY TO DEPOLARIZE WHEN ISCHEMIC

After a stroke: SEIZURES After an MI: ARRYTHMIAS After ischemic bowel: BLOODY DIARREA After a DVT: CRAMPS

WITH Na and Ca trapped within the cell

Since atria use Ca to depolarize, the trapped Ca may cause atrial arrythmias

Contractility of muscles increases

WITH CELL DYING, Sodium continues to accumulate inside

cell Chloride will follow WATER will follow next SWELLING is therefore the FIRST visible

change of cellular injury

SWELLING

Cerebral edema Papilledema Hydropic changes Dilated lymphatics Third spacing

INFLAMMATION TIME LINE < 24 hours: SWELLING AT 24 hours: NEUTROPHILS show up

and peak at 3 days T-cells and MACROPHAGES: show up at

day 4 and peak at day 7 FIBROBLASTS: show up at day 7, peak at

day 30, and take 3 to 6 months to complete their work ( chronic inflammation)

WHEN TOO MUCH SODIUM INSIDE CELL.

Sodium begins to leak OUT of the cell now that concentration gradient is reversed

The only way for sodium to get out is to use the Na-Ca exchange protein which is concentration driven

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IF BLOOD SUPPLY NEVER RETURNS TO THE CELL

The sodium can pull ALL the calcium into the cell

WHILE calcium is moving into cell, more atrial arrythmias may develop

WHEN ALL CALCIUM NOW TRAPPED WITHIN THE CELL

Cells that depend on EXTRACELLULAR calcium will lose function SMOOTH MUSCLE ATRIUM VENTRICLE

SIGN OF CHRONIC DISEASE

ON BIOPSY: you see evidence of fibrosis ON X-RAY: you see calcifications ALL inflammatory processes

DONE!!!

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Electrolyte Physiology

Something in the way she moves me

Electrolyte Movement CONCENTRATION GRADIENT ELECTRICAL GRADIENT DRIVING FORCE NERNST NUMBER (E-ion) CONDUCTANCE (G-ion) PERMEABILITY










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Electrolyte Movement Depolarize: to become positive from

baseline Overshoot: more positive than the

threshold potential Repolarization: to become negative from a

positive potential Hyperpolarization ( or undershoot): to

become more negative than baseline potential

Sodium Channels

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HEART BLOCKS NORMAL PR-interval :

HEART BLOCKS, cont THIRD DEGREE HEART BLOCK

COMPLETE AV DISSOCIATION AV-node has INFARCTED P-waves and QRS complexes have NO

relationship ALL must have a pacemaker

QRS COMPLEXES Premature ventricular complex (PVC)

No P- wave; wide QRS complex; a pause following the QRS complex

BIGEMINY: A PVC every other beat TRIGEMINY: A PVC every third beat VENTRICULAR TACHYCARDIA: three or

more consecutive PVCs with a minimum heart rate of 150

VENTRICULAR FIBRILLATION: NO recognizable QRS complexes

VENTRICULAR TACHYCARDIA IF PATIENT STABLE: treat with

medication IF PATIENT UNSTABLE:

SHOCK with 200joules SHOCK with 300joules SHOCK with 360(max)joules LIDOCAINE SHOCK BRETYLIUM or AMIODORONE

VENTRICULAR FIBRILLATION EPINEPHRINE TREAT LIKE VENTRICULAR

TACHYCARDIA

ATRIAL ARRHYTHMIAS Premature atrial contraction (PAC) Multifocal atrial tachycardia Paroxysmal supraventricular tachcardia Atrial flutter Atrial fibrillation

If ACUTE and STABLE: treat with medication If ACUTE and UNSTABLE: DEFIBRILLATE If CHRONIC: treat medically; put on coumadin May defibrillate after minimum 2 weeks on coumadin

TX: use synchronized button

ELECTROLYTES AFFECT DEPOLARIZATIONS

FOUR SPECIALIZED MEMBRANES NEURONS SKELETAL MUSCLES SMOOTH MUSCLES CARDIAC MUSCLE

ATRIUM: uses calcium to depolarize VENTRICLE: uses sodium to depolarize; uses

intracellular calcium to contract; depends on extracellular calcium to trigger off intracellular calcium release

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HYPERMAGNESEMIA LESS LIKELY TO DEPOLARIZE AFFECTS CALCIUM AND POTASSIUM GETS IN THE WAY OF SODIUM TX: IV normal saline; loop diuretic

HYPOMAGNESEMIA MORE LIKELY TO DEPOLARIZE AFFECTS CALCIUM and POTASSIUM AFFECTS all KINASES TX: magnesium sulphate

HYPERCALCEMIA LESS LIKELY TO DEPOLARIZE

everywhere except the atrium( more likely) SMOOTH MUSCLE: initially less likely

(blocks nerve) to depolarize, then more likely to CONTRACT (due to second messenger systems)

TX: IV normal saline; loop diuretics

HYPOCALCEMIA MORE LIKELY TO DEPOLARIZE

everywhere except the atrium( less likely) WILL AFFECT SECOND MESSENGER

SYSTEMS SMOOTH MUSCLE: initially more likely to

depolarize( nerve fires more) followed by less likely to CONTRACT (affects second messenger systems)

HYPERKALEMIA Initially MORE LIKELY TO DEPOLARIZE Potassium will flow into the cell, taking the

membrane potential closer to threshold Potassium gets trapped INSIDE the cell during

repolarization; repolarization therefore takes longer > LESS LIKELY TO DEPOLARIZE Peaked T waves Widened T waves Prolonged QT interval

Predisposes to arrythmias

HYPOKALEMIA LESS LIKELY TO DEPOLARIZE Potassium will rush out of the cells,

making them more negative Cells repolarize even faster Cells repolarize too much

Narrow T waves Flat T waves Flipped and inverted T wave The U wave( exaggerated flipped T wave)

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HYPERNATREMIA MORE LIKELY TO DEPOLARIZE SODIUM rushes into the cells, making

them more positive After sometime, the NA-K ATP-ase kicks

Into high gear, making the cells more negative( less likely to depolarize)

TX: IV normal saline; correct slowly

HYPONATREMIA MORE LIKELY TO DEPOLARIZE SODIUM will now leak out of a cell by Na-K

exchange When calcium leaks INTO cell in exchange for

sodium leaking OUT, cells become more positive

TX: IV normal saline; correct slowly Use 3% saline if sodium under 120 with symptoms Use fluid restriction if hyponatremia due to SIADH

Hyponatremia The End: Turn off the lytes

Antiarrhythmics Class 1: Na channel blockers 1a

Quinidine Procainamide Disepyramide

1b Lidocaine Tocainide Mixelitine Phenytoin

1c Encainide Flecainide propofenone

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Class II: Beta Blockers All end in lol Specific beta 1: begins with A thru M, but

NOT L or C Nonspecific: begins with N thru Z,

including L and C

Class II: Beta Blockers Propanolol Acebutalol Esmalol Atenalol Sotalol Pindalol Timalol Butexalol Labetalol Carvedilol

Class III: K Channel blockers Napa ( from procainamide) Sotalol Bretylium Amiodorone

Class IV: Ca Channel blocker Verapamil Quinidine Diltiazem Procainamide Nifedipine Phenytoin Nicardipine Nimodipine Femlodipine Amlodipine

IF YOU PLAY WITH LYTES You may go down IN FLAMES

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PULMONARY PHYSIOLOGYTAKING A DEEP BREATH

PULMONARY PHYSIOLOGY

Foregut Endoderm Respiratory Tract GI Tract > from the mouth to the second

part of the duodenum

Neural Crest Tracheal cartilage Laryngeal cartilage

Embryogenesis Develops in the first trimester like every

other organ Surfactant production is NOT complete

until approximately 32 to 34 weeks Brain develops first in embryo: notochord

visible by 3 weeks; brain formed by 8 weeks

Surfactant Decreases atmospheric pressures effect

on the alveoli > PREVENTS ATELECTASIS

Increases compliance of alveoli

Compliance = change in volume / change in pressure

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You know surfactant production is complete when

Lecithin / sphyngomyelin ratio is 2:1 or greater or

You detect phosphatidylglycerol, a breakdown product of surfactant

If mom comes in with preterm labor

Check L / S ratio Check for phosphatidylglycerol

If both of the above are negative Beclamethasone Betamethasone If baby still born early, then there is synthetic

surfactant that can be applied

When there was NO surfactant Alveoli would collapse: Atelectasis > leads to very poor compliance > increases work of breathing > weakness and shortness of breath > oxygen is given > oxygen has difficult time diffusing across > oxygen builds up, causing free radical

formation > alveoli develop hyaline membrane in order to protect themselves

Restrictive Lung Disease Have poor

compliance Have trouble

breathing in Have poor diffusion Have increased A-a

gradient pO2 =low pCO2 =low

pH =high

Develop a secondary perfusion problem

LOW ENERGY state LOW VOLUME state ALL die from heart

failure known as COR PULMONALE = right sided heart failure due to pulmonary HTN (severe RVH)

Hyaline Membrane Disease

THE FIRST RESTRICTIVE LUNG DISEASE

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COMPLICATIONS of HMD ( or RLD) As compliance drops, the need for

pressure support increases As diffusion decreases, the need for

oxygen increases More oxygen means more free radicals,

which means more hyaline membrane Bring in the JET VENTILATOR

Complications, cont More pressure support can lead to a

PNEUMOTHORAX Kussmaul sign: increased JVD on inspiration Pulsus paradoxicus: exaggerated drop in BP

( more than 10mm) or in pulse rate ( more than 10 bpm)

Loss of pulse and BP Cyanosis Hammans sign: subcutaneous emphysema

Pneumothorax Spontaneous Traumatic

Asymptomatic symptomatic

As free radicals traumatize the AIRWAY

Airway produces mucus to protect itself Airway thickens Goblet cell hyperplasia Airway lumen narrows Increased REID index BRONCHOPULMONARY DYSPLASIA

The first obstructive lung disease

Obstructive Lung Disease Difficulty breathing OUT Problem with VENTILATION ABG: pO2 = nl or low pCO2 = high pH=low Too much airway mucus Airway thickening Goblet cell hyperplasia Increased Reid Index Mcc of death is BRONCHIECTASIS

EVERY lung disease presents with the SAME signs and symptoms!!!

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Can it really be this easy???

Amniotic Fluid Production 80% is a filtrate of moms plasma To SUBTRACT:

Swallow ( a reflex) Digest ( need patent UGI)

20% comes directly from the fetus To ADD:

Process the swallowed fluid, then add 20% more than was swallowed, then URINATE

Role of Amniotic Fluid Main function is shock absorption Secondary action is to prevent

atmospheric pressure from affecting the fetus, especially the lungs

Problem with amniotic fluid POLYHYRAMNIOS

Autonomic dysfunction ( Riley-Day syndrome)

Neuromuscular disease ( Werdnig-Hoffman syndrome)

UGI atresia Esophageal atresia Duodenal atresia

OLIGOHYDRAMNIOSRENAL agenesis or obstruction

Potters Syndrome When OLIGOHYDRAMNIOS leads to

pressure effects on the fetus ( everything is flattened)

Will lead to pulmonary aplasia or hypoplasia due to the positive pressure

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Prune Belly Syndrome Absence of abdominal wall musculature Fetus is unable to urinate in utero Fetus is unable to bear down and raise

abdominal pressure for urination OLIGOHYDRAMNIOS

Unable to urinate due to neuromuscular weakness? Teach to (self) catheterize

It is important to have negative pressure in the thoracic cavity!

Diaphragmatic Hernias The diaphragm forms from Ventral to

Dorsal

Bochtalek defect: rear defect Morgagni defect: anterior, midline defect

Visible by sonography in utero Bowel sounds in chest exam

Must repair surgically immediately after birth

Extrathoracic Airway From the lips to the glottis Narrows on inspiration; expands on

expiration NOT protected by the thoracic cage

Intrathoracic Airway From the glottis to the alveoli Expands on inspiration; narrows on

expiration Protected by the thoracic cage Has a vacuum surrounding it

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Trachea Has 16 to 20 C-shaped cartilage rings,

with the opening to the C facing posteriorly This allows partial collapse of the airway

during swallowing to prevent aspiration Has three anatomic narrowings

The glottis Midway: due to anterior compression by aorta Carina: located at T4 (level of nipple)

Aspiration If patient is unable to speak, then the

object is lodged in the trachea LARGE OBJECTS tend to lodge at the

glottis 90% of time Perform the Heimlick Maneuver Perform Back Thrusts if less than 2 y/o If still unable to dislodge the object

Perform emergency cricothyroidotomy

Aspiration, cont Small objects tend to lodge in the right

lower lobe Recurrent RLL pneumonia: R/O FB aspiration

Do inspiratory-expiratory films Right mainstem bronchus is larger and

straighter than the left If person is sitting or standing UP, the object will

lodge in the superior segment If patient is lying DOWN, the object will lodge in the

posterior segment

Evaluation for aspiration Inspiratory film: all lobes are inflated Expiratory film: the lobe with the aspirated

object does NOT collapse Tx: bronchoscopy

Airway Anatomical Divisions Dead space Respiratory unit

Dead space ventilation Alveolar ventilation Total ventilation

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Histology Pneumocytes

Type 1: macrophages Type 2: produce surfactant

Goblet cells: produce mucus to trap debris Mucus moves 1 inch per cough

Smooth muscle Clara dust cells cartilage

Epithelium Upper 1/3 of trachea has squamous cells Mid 1/3 of trachea is a combination Main respiratory epithelium is tall columnar

ciliated epithelium The more you smoke, the longer the zone

of squamous cells

Cilia Line the entire airway Beat in one direction > orad Has the 9 + 2 configuration (9

microtubules surrounding 2 actin proteins) Need a Dynein arm to have flexibility

Kartageners Syndrome Dynein arm is defective An obstructive lung disease

Bronchiectasis Infertility Situs Inversus

Lung Sounds Stridor: narrowing in extrathoracic airway Wheeze: narrowing in intrathoracic airway Rhonchi: air moving over mucus Crackles: collapsed airways popping

open Surfactant is missing Alveoli have been scarred down

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Lung Sounds, cont Decreased breath sounds: space between

alveolus and chest wall is occupied Dullness to percussion: as above Increased fremitus: consolidation on same

side or atelectasis on opposite side Bronchophony, egophony, or e to a

changes: as above

Lung Sounds, cont Tracheal deviation: towards atelectasis

and away from a pneumothorax Hyperresonance: pneumothorax on same

side or atelectasis on opposite side

Lung Infections Croup Bronchiolitis Bronchitis

Acute chronic

Pneumonia Airway interstitial

tracheitis

Airway Infections Epiglotitis: H. Influenza B Tracheitis: C. Diptheria Pneumonia

Rusty colored sputum: Strep Pneumonia Curant jelly sputum: Klebsiella Pneumonia Sulphur granules: Actinomyces Israelii Frequent after the flu: Staph Aureus Malodorous smell or gas formation:

Anaerobes

Interstitial Pneumonias Atypicals

Chlamydia: from 0 to 2 mo Mycoplasma: from 10 to 30 y/o Legionella: over 40 y/o

Fungus Histoplasmosis: midwest Blastomycosis: northeast Coccidiomycosis: southwest

Interstitial pneumonias Fungus, cont

Paracoccidiomycosis: South America Aspergillus: moldy hay or moldy basement Sporothrix: rose thorn

Pneumoconioses Asbestosis Silicosis Bissinosis berrylliosis

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Interstitial pneumonias, cont Nocardia: the only G+ that is partially acid

fast Sarcoidosis: noncaseating granulomas;

large hilar adenopathy; high ACE levels

Lung Masses Most common MASS in children:

hamartoma Most common MASS in adults:

granulomas Most common TUMOR: adenoma

Central Cancers Squamous Cell Carcinoma: produces PTH Small Cell Carcinoma

Anaplastic Located at the carina Produces 4 hormones:

ACTH: 90% ADH: 5% PTH: 3% TSH: 2%

Peripheral Cancers Bronchogenic adenocarcinoma Bronchioalveolar adenocarcinoma

Carcinoid syndrome flushing, wheezing and diarrhea Too much serotonin Measure 5-HIAA in the urine

Large cell adenocarcinoma

Risk factors for lung cancer Primary smoking

Risk increases with amount AND duration If you STOP smoking: 5 yrs > reversal of

damage visible; 15 yrs > risk back to baseline Radon Second hand smoke

(1) sidestream smoke (2) mainstream smoke Pneumoconioses

Time for the PHYSIOLOGY of the lung!!

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Three PHYSIOLOGIC parts to the lung

Intrathoracic space Chest wall Pleural space

Pulmonary vasculature Pulmonary airway

Lung Volumes RV: the amount of air left in the lungs AFTER

forced expiration Can not be physiologically forced out Maintains some compliance in the airway

ERV: the amount of air that can still be FORCED out AFTER a normal exhalation Fills up the dead space; decreases the tidal volume

that you would have to take in

FRC: a combination of RV and ERV

Lung Volumes, cont TV: the amount of air you take IN during a

NORMAL inhalation effort

IRV: the amount of air you can FORCE INSPIRE after a normal inhalation effort

TLC: ALL the air in your lungs at the END of a deep breath ( RV + ERV +TV + IRV)

VC: all the air you can breathe in AFTER forced exhalation ( ERV + TV + IRV)

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Compliance and Air Flow Inspiration Beginning: expansile forces of the CHEST

WALL is greater ( 0 to 49%) Middle: expansile forces of the LUNG is

greater ( 50 to 99%) End: recoil force of the chest wall

EQUALS the expansile force of the lung

Expiration Beginning: recoil forces of the CHEST

WALL are greater ( 0 to 49%) Middle: recoil forces of the LUNG are

greater ( 50 to 99%) End: the recoil force of the lung EQUALS

the expansile force of the chest wall

Breathing in FRC: baseline > intrathoraxic pressure is

negative ( - 3 to 5) TV: intrathoraxic pressure gets more

negative ( -10 to -12) TLC: intrathoraxic pressure most negative

(-20 to -25) Intrathoraxic Pressure should always be

NEGATIVE

Intrathoracic Pressure Intrathoraxic Pressure

Should ALWAYS remain negative Should decrease with inspiration If it gets positive, then it will resist any

blood or air from entering the thorax If you do not breathe in, there will be NO

pressure gradient for blood to enter the thorax

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Positive Intrathoracic Pressure Kussmaul sign: increased JVD with

inspiration Pulsus paradoxicus: exaggerated drop in

BP( more than 10mmHg) or pulse ( more than 10bpm) on inspiration

Mcc: pericardial tamponade or pneumothorax

Pericardial Tamponade Mcc: trauma or cancer CXR: enlarged cardiac shadow ECHO: compressed small heart Tx: pericardiocentesis If recurrent: put in a pericardial window

Pneumothorax Traumatic Spontaneous

Associated with estrogen use or collagen disease

Less than 25% occupation & asymptomatic More than 25% occupation or symptomatic

Tx: chest tube placement

Pulmonary Vasculature Flow ( Q ) As you breathe in, the lung Inflates, pulling

on traction fibers attached to vessels As vessels DILATE, flow increases As flow increases, oxygen dilates the

vessels, significantly increasing Q The increased Q keeps the pulmonary

valve open longer, INCREASING S-2 splitting

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Flow ( Q ) is greater to the bottom of the lungs because

(1) gravity (2) less resistance (3) more oxygen goes to the bottom of the

lungs with each breath Normal RR = 12 to 16 breaths/min

Q increases on inspiration and decreases on expiration.

S-2 Splitting Increases on inspiration due to Increased

pulmonary blood flow Decreases on expiration due to decreased

pulmonary blood flow This is why RIGHT sided heart sounds

increase on INSPIRATION This is why LEFT sided heart sounds

increase on EXPIRATION

Oxygenation Directly related to DIFFUSION and

PERFUSION More oxygenation is accomplished at the

bottom of the lungs only on inspiration Most of oxygenation is accomplished at

the top of the lungs > ALWAYS OPEN!

Ventilation (V) Inversely related to pCO-2 Definition: patent airway Measurement: pCO-2 ( on ABGs)

More V to the bottom of the lungs only on inspiration

Most V at the top of the lungs because it is ALWAYS PATENT

The Law of V / Q V /Q is greatest at the top of the lungs,

equally matched in the middle, least at the bottom

If you change one, you MUST change the other in the SAME direction

ANY V / Q mismatch will lead to hypoxia

Pulmonary Airway

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Pulmonary Airway Pressure

The Only Pressure That Gets Positive With Each Breath

How The Brain Monitors Pulmonary Physiology Signals from the lungs and chest wall

J-receptors: found in the interstitium of lungs Senses interstitial particles Increases respiratory rate

Slow adapting receptors: found in the ribs, especially the sternocostal junctions Senses stretch and inflation Causes exhalation

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SINUSES Maxillary Ethmoid Sphenoidal Frontal

BODIES AORTIC BODY: found in the arch of the

aorta Measures pCO-2, pH, and H+ ions

CAROTID BODY: located at the bifurcation of the internal and external carotids Measures PO2, PCO2, pH, and H+ ions

BRAIN More sensitive to elevated pCO-2 Hypoxia and Hypercarbia are synergistic Forms of pCO-2:

90% in the form of HCO-3 7% as carbaminohemoglobin and

carboxyhemoglobin 3% is dissolved ( .03pCO2 )

Medulla Responsible for BASIC functions; has a

RR of 8 to 10

BRAIN DEAD: no function above the medulla

COMATOSE: cerebral cortex is still alive, but patient unable to respond

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Pons RESPONDS to the environment Locked-In syndrome: damage to pons; patient

only able to blink as response Most sensitive to osmotic shifts > Central Pontine

Demylinolysis

Apneustic center: senses hypoxia; causes inspiration

Pneumotactic center: senses hypercarbia; causes exhalation

Kussmaul Breathing RAPID, DEEP breathing Means METABOLIC ACIDOSIS

Apneustic Breathing Pneumotactic center is desensitized, as in

COPD A lesion below the pneumotactic center

but above the apneustic center

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Apnea Central Apnea: NO inspiratory effort, with or

without bradycardia, in 20 seconds or more Apnea monitor Tx: Caffiene; theophylline

Obstructive Apnea: occlusion of airway during sleep, usually caused by obesity Weight loss Progesterone CPAP Surgery: Uvulopalatoplasty

Lesions to MEDULLA

Lesions to MEDULLA Hypoglycemia Ischemia

Thoracic outlet syndrome Subclavian steal syndrome

THE END

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And now for a few good CLUES Obstructive Lung Diseases Bronchitis

Acute chronic

Bronchiolitis Asthma

Intrinsic extrinsic

Cystic fibrosis Bronchiectasis

Emphysema Panacinar Centroacinar Distoacinar Bullous

Staph aureus Pseudomonas

Really! The End!!

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NEUROMUSCULAR PHYSIOLOGY

I WANT A CONTRACT

NEUROLOGICAL CONTROL

Central Nervous System Involves the BRAIN and SPINAL CORD

PARASYMPATHETIC system Controls the craniosacral divisions

SYMPATHETIC system Controls the thoracolumbar divisions

Inhibitory Neurotransmitters GABA: brain; causes an influx of chloride

GLYCINE: spinal cord; causes an influx of chloride

PARASYMPATHETIC SYSTEM

Uses acetylcholine for preganglionic fibers and postganglionic fibers

DEPOLARIZES the head and neck as well as below the belt

HYPERPOLARIZES the thoracolumbar areas

Has long preganglionic fibers, short postganglionic fibers

SYMPATHETIC SYSTEM

Uses acetylcholine for preganglionic fibers; uses primarily NE for postganglionic fibers

Some pathways use DA or SEROTONIN DEPOLARIZES the brain and the

thoracolumbar areas HYPERPOLARIZES the sacral area Has short preganglionic fibers, long

postganglionic fibers

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Second Messengers

PARASYMPATHETIC: c-GMP SYMPATHETIC: c-AMP

Smooth muscle contraction by neurotransmitter or hormone: IP3/DAG

Smooth muscle contraction by distention: calcium-calmodulin

Parasympathetic Receptors Most are MUSCARINIC except at ganglia

or neuromuscular junctions which are NICOTINIC

Sympathetic Receptors Many are NICOTINIC, except for sweat

glands which are muscarinic or

Alpha 1 Receptors Arteries: vasoconstriction Sphincters: tighten Radial muscles of the eyes: mydriasis w/o

cycloplegia

Alpha 2 Receptors All presynaptic sympathetic fibers: inhibit

NE release Islet cells of pancreas: inhibit insulin

secretion

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Beta 1 Receptors CNS: increased activity SA NODE: increase heart rate and

contractility JG Apparatus: increased renin release Alpha cells of pancreas: increased

glucagon release

Beta 2 Receptors CNS: increased activity Ventricles: increased contractility but NOT

rate Lungs: bronchodilation Arterioles: vasodilation Islet cells of pancreas: increased insulin Uterus and Bladder: relaxation

If you want to stimulate You want to depolarize Make the cell more positive Make Na move INTO the cell Make Ca move into SA node

If you want to inhibit CNS: make CL move into cell PNS: make K move out of cells

In either case, cells become more NEGATIVE and are less likely to depolarize

NOW FOR THE MUSCLES! TYPES of MUSCLES CARDIAC muscle SKELETAL muscle SMOOTH muscle

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STRIATED MUSCLES Cardiac muscle Skeletal muscle

Striations due to sarcomeres

Smooth Muscle Appear smooth due to lack of striations

Skeletal Muscle Use intracellular calcium for contraction 100% electrochemically coupled Function as motor units( one nerve fiber

and all the muscle fibers it innervates Demonstrate RECRUITMENT NO AUTONOMICS NO SYNCYTIAL activity

Cardiac Muscle Uses intracellular calcium for contraction Needs extracellular calcium to trigger off

intracellular calcium release Complete SYNCYTIAL activity The most gap junctions Complete AUTONOMICS Can function without innervation,

neurotransmitters or hormones

Smooth Muscle Uses intracellular calcium for contraction Needs extracellular calcium for its second

messenger system ( when it flows inside the cell)

Has AUTONOMICS Has partial SYNCYTIAL activity Can function without innervation,

neurotransmitters or hormones

NEUROMUSCULAR TRANSMISSION

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MUSCLE CONTRACTION Calcium binds trop-C Trop-C releases trop-I Trop-I releases

tropomyosin Tropomyosin releases

actin binding sites

Myosin heads bind actin CONTRACTION occurs

Myosin heads release ADP from previous rd

Myosin heads bind new ATP

Myosin heads hydrolyze ATP

RELEASE occurs Myosin heads return

to start position

MUSCLE CONTRACTION, cont Tropomyosin binds actin Trop-I binds tropomyosin Trop-C binds trop-I Ca-ATPase pumps Ca back into SR Phospholambin inhibits Ca-ATPase when

it is done pumping

Clinical Application

Diagnosis of a Myocardial Infarction

EKG: Na-K pump stops > peaked T-wave > ST-wave depression > ST-wave elevation > T-wave depression, then inversion > Q-wave

Troponin I: rises at 2 hours > peaks in 2days > positive up to 7 days

CK-mb: rises in 6 hours > peaks in 12 hours > gone in 24 to 36 hours

LDH 1: rises in 24 hours > peaks in 48hours > gone in 72 hours

Management of an MI 24 hour hospitalization Check EKG Q6 Check CIEs Q6 Monitor for arrythmias Discharge after 24 hours IF asymptomatic Re-evaluate in 6 weeks

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In 6 Weeks Exercise stress test

Positive IF: chest pain is reproduced; ST-wave changes; drop in BP

Stress Thallium test A perfusion test; looking for a COLD spot

Dobutamine or Dipyridamole stress test Use when patient unable to exercise

Calcium Pyrophosphate scan Taken up by DEAD tissue; looking for HOT spot

2-D echo Evaluates anatomy of heart; measures SV and CO

The Functional Unit of Muscles

THE SARCOMERE

MUSCLE DIFFERENCES

CARDIAC MUSCLE In addition to wave of depolarization,

calcium MUST flow into the T-tubules during phase 2 for contraction to occur

Ventricle depends on EXTRACELLULAR calcium to trigger its contraction

Smooth Muscle Has NO sarcomeres Contains NO troponin > actin and myosin

are always bound ( LATCHING) Contains BASAL BODIES Has NO myosin ATPase activity

Has MLCK and MLCP working together

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As Muscle Contracts LENGTH decreases FORCE and TENSION increase A band stays the same Amount of OVERLAP increases The H band and I band therefore shrink

Length/Tension Curve

Golgi Tendon Organs Located at muscle insertions Monitor the force of muscle contractions Allows muscle to hold MAXIMUM muscle

contraction force for only one second Once it fires, muscle fibers MUST relax Prevents destruction of sarcomeres

Muscle Strain Overstretching or tearing a muscle When a muscle is torn, it goes into spasm

to keep the fibers together for proper healing Tx: rest it > apply heat > NSAIDS > muscle

relaxants

JOINT SPRAIN TORN tendon or ligament

Tx: Rest it > Ice Compression > Elevate the extremity

Frank-Starling Curve

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Congestive Heart Failure Over 50% mortality in 5 years Most common medicare diagnosis Muscle fibers are overstretched Dilated ventricle Increased EDV and ESV Decreased contractility > decreased CO

and EF

Congestive Heart Failure after a myocardial infarction

AT LEAST 40% of myocardium lost EJECTION FRACTION is less than 45% Due to left coronary artery infarcts 90% of

time

Treating CHF: Applying Frank-Starling Curve

Decrease volume Restrict sodium intake Restrict volume intake

Increase contractility Digitalis Dobutamine Dopamine

Decrease TPR Ace inhibitors

NEUROMUSCULAR PROFILE

ALL YOU NEED NOW IS THE CLUE Inflammatory Myopathies

Myositis Polymyositis Dermatomyositis Fibrositis Fibromyalgia Polymyalgia

rheumatica Temporal Arteritis

ALL HAVE: High ESR High WBC count Myoglobinemia High AST, ALT and

Aldolase

112112

Muscular Dystrophies Duchennes

Gowers sign Waddling gait Pseudohypertrophy of the calf Dystrophin protein X-linked recessive; onset BEFORE age 5

Beckers Onset AFTER age 5

Myotonic

Neuropathies Guillian Barre Diabetes mellitus Syphilis Myesthenia Gravis / Myesthenic or Eaton

Lambert syndrome

Acetylcholinesterase inhibitors: reversible

Edrephonium Neostigmine Pyridostigmine Physostigmine

Acetylcholinesterase inhibitors: irreversible

AKA Organophosphates End in .phate ( diflorophate; echothiophate) End in .thion ( malathion; nalathion;

parathion)

If they come back complaining about more weakness

Myesthenia Gravis has gotten worse or Cholinergic crisis

REPEAT EDREPHONIUM TEST!! IF patient gets better > disease is worse

Increase neostigmine IF patient gets worse > cholinergic crisis

Hold neostigmine > give atropine > decrease neostigmine

Anticholinergic Drugs Side effects are sympathetic except for HOT, DRY SKIN!

Atropine Glycopyrollate Pilocarpine Benztropine Trihexyphenidyl ipratropium

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Neoplastic Associations Myesthenia Gravis: THYMOMA

Myesthenic syndrome: SMALL CELL CARCINOMA; a paraneoplastic syndrome Sarcoplasmic reticulum is slow to sequester

calcium; cancer blocks some calcium channels

Neuropathies, cont Multiple sclerosis Metachromatic leukodystrophy

Treatment of MS STEROIDS IV GAMMGLOBULINS PLASMAPHARESIS

Lower Motor Neuron Disease Amyotrophic lateral sclerosis Werdnig-Hoffman Disease Polio

Cerebellar Disease in 5 to 10 Y/O children

Ataxia Telangiectasia Fredricks Ataxia Adrenoleukodystrophy

Cerebral Palsy Any permanent neurological damage suffered

PRIOR to age 21 years

Spastic Diplegia Midline cortical problem

Spastic Hemiplegia Cortical problem on ONE SIDE of the brain

Choreoathetosis BASAL GANGLIA is involved: kernicterus

Atonic FRONTAL CORTEX: involves the CST

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THE END

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VASCULAR PHYSIOLOGYYOU GOTTA HAVE SOME FLOW

Im Talking About SMOOTH

SMOOTH MUSCLE, that is

Smooth Muscle THICKEST layer of smooth muscle is

found in the aorta MOST smooth muscle by surface area

found in the arterioles LEAST smooth muscle found In the veins

and veinules

Arterioles Considered the STOPCOCKS of the

vascular tree MOST smooth muscle by surface area

allows most vasodilatation and vasoconstriction

Maintain AUTOREGULATION Do the MOST to regulate BP, up or down

AUTOREGULATION Between BP 60 to 160 systolic : cerebral,

coronary, and renal perfusion remains constant

ISCHEMIC infarct: BP went below 60 systolic

HEMORRHAGIC infarct: BP went above 160 systolic

Veins and Veinules Have the most CAPACITANCE Have the least smooth muscle 60% of blood ( the most) is pooled here Depend on skeletal muscle contractions to

squeeze blood upward Have one-way valves which move blood

from superficial to deep veins

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CONTROL of vessels VEINS: under parasympathetic control This is why veins are usually dilated Blood flow rate is quite slow example: subdural hematomas

If Hypovolemia Develops VENOCONSTRICTION is first response to

loss of volume > gets volume back into circulation

Venoconstriction is most significant in skin and GI Poor skin turgor Loss of bowel sounds and ileus

A-V Anastamoses Shunt blood away from nonessential

organs More concentrated in fingertips, tips of

toes, tip of nose, lips and earlobes Severe vasoconstriction hypothermia

CONTROL of vessels, cont ARTERIES: under sympathetic control This is why arteries are usually constricted Reactive hyperemia: cutting an artery or

the nerve to that artery causes immediate vasodilatation

i.e. epidural hematoma

Receptors ARTERIES: alpha one ( IP3/DAG)

vasoconstriction ARTERIOLES: beta 2 ( c-AMP)

vasodilatation VEINS: alpha 1 ( IP3/DAG)

venoconstriction

Capillaries Have the thinnest membranes Made for diffusion Have the greatest surface area

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As Blood Flows Through the Capillaries

Fluid diffuses out; large proteins (albumin) stay in

Osmotic pressure rises in the capillaries Concentration gradient pushes particles

out of capillaries

In the Veins and Venules Osmotic pressure is now high enough to

PULL waste products into vessels Blood PULLS waste products back into

circulation

Total Pressure in a vessel As a Vessel Narrows Velocity increases Flow decreases Resistance increases Blood Pressure rises

Resistance in Series

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Resistance in Parallel During Diastole Ventricles are relaxing Very LOW RESISTANCE in coronaries Aortic valve is closed Aorta has MORE TRANSMURAL

PRESSURE

MORE CORONARY BLOOD FLOW

During Systole Ventricles are CONTRACTING There is HIGH RESISTANCE in coronary

vessels Velocity in aorta is too high Aortic valve is open LOW TRANSMURAL PRESSURE

LESS CORONARY BLOOD FLOW

In Summary LESS blood flow through coronary arteries

during SYSTOLE MORE blood flow through coronary

arteries during DIASTOLE Most work is done in systole! A-V O2 difference created during systole Therefore: MOST O2 EXTRACTION

occurs in systole

A-V O2 Difference At REST: the heart extracts 97% of O2 With EXERCISE: skeletal muscle After EATING: GI system During INTENSE CONCENTRATION: the

brain

LOWEST A-V O2 difference: the kidneys, at all times

Lets Look at FLOW

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POISSOILE LAW

Regulation of Radius CNS: pCO2 pO2 LUNGS: pO2 MUSCLES: pCO2 pH CV: adenosine SKIN: temp pCO2 GI: food, especially fats RENAL: PGE2; dopamine; ANP

NEUROLOGICAL control of blood pressure

Carotid Sinus Located at the bifurcation of the common

carotid Responds to FLOW or STROKE VOLUME Increased STRETCH means increased

FLOW Sensory nerve : CN IX Efferent nerve : CN X

REMEMBER! Stroke volume, carotid sinus stretch, CN

IX firing and CN X firing ALWAYS go in the same direction

CN IX and CN X are ALWAYS firing Amount of firing varies always in SAME

DIRECTION as the stroke volume

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Autonomic Dysfunction Mcc: DIABETES MELLITUS In Newborns: Riley-Day syndrome In Parkinsonism: Shy-Dragger syndrome In elderly: Sick Sinus syndrome

Low Volume State Low stroke volume >

low carotid stretch > low CN IX firing > decreased CN X firing >increased heart rate > increased NE from NTS in medulla > increased TPR > decreased RBF > decreased GFR >

> increased renin, angiotensinogen, aldosterone secretion > increased Na reabsorption > increased total body Na > decreased urinary Na > decreased FENa > increased urinary K > > > >

Low Volume State Decreased serum Na( dilutional) Decreased serum Cl ( dilutional) Decreased serum K (real and dilutional) Decreased urine pH ( aldosterone

excretes H) Increased serum Ph (metabolic alkalosis) Increased TPR

Most common cause of hyponatremia?

LOW VOLUME STATE

Most common cause of hypokalemia?

LOW VOLUME STATE

121121

Most common cause of hypochloremia?

LOW VOLUME STATE

Most common cause of high TPR ? LOW VOLUME STATE

Most common cause of metabolic alkalosis?

LOW VOLUME STATE

ALKALOSIS favors calcium precipitation with phosphate KIDNEY STONES !!!!

Ace Inhibitors Stop conversion of AT-1 to AT-II Increased bradykinin VASODILATION and VENODILATION Decreased preload and afterload BALANCED dilation Contain sulphur Decrease mortality in CHF; decreases

proteinuria in diabetic nephropathy

Ace Inhibitors

Captopril Lisenopril Enalopril rinilopril

Angiotensin Receptor Blockers Losartan Vosartan

Do not contain sulphur NO elevation in bradykinin

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What is a VASCULITIS? Vasculitis Schistocytes ( Burr cells; helmet cells) Petechiae, purpura and ecchymoses LOW ENERGY STATE LOW VOLUME STATE Restrictive lung disease profile CELL MEDIATED inflammation

All You Need Now is the Clue!!! Ig-A nephropathies Bergers Henoch-Schonlein Purpura Alports

More vasculitides Buergers DIC HUS TTP DM Syphilis Takayasu kawasaki

More vasculitides Temporal arteritis Ankylosing Spondylitis PAN Wegeners Goodpastures Leukocytoclastic Churg-Strauss

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Collagen Vascular Diseases CREST syndrome Scleroderma Progresive Systemic Sclerosis MCTD RA / JRA (Stills disease)

Feltys: RA & leukopenia and splenomegaly Becets : RA & GI ulcerations Sjogrens : RA & xeropthalmia, xerostomia

Collagen Vascular Diseases with LOW COMPLEMENT

PSGN Serum Sickness SBE SLE MPGN : type l, ll Cryoglobulinemia

THIS IS THE END

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CARDIAC PHYSIOLOGYTHE HEART OF THE MATTER

PRESSURE is the GRADIENT of the organs! OPENING SNAP

A valve is popping open during diastole TRICUSPID STENOSIS MITRAL STENOSIS

EJECTION CLICK A valve is popping open during systole

AORTIC STENOSIS PULMONARY STENOSIS

MIDSYSTOLIC CLICK Blood is coming at high velocity, slapping

the mitral valve on the way out Occurs closer to S-1 with standing and

closer to S-2 with lying down MITRAL VALVE PROLAPSE

Occurs in 7% of normal women (estrogen connection)

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SOFT S-1 One of the two valves that contribute to

this sound is NOT closing

TRICUSPID REGURGITATION MITRAL REGURGITATION VALVE IS NOT THERE!

Tricuspid atresia Mitral atresia

BOTH ARE CYANOTIC

LOUD S-1 Either you have a stiff valve that bangs

shut: TRICUSPID or MITRAL STENOSIS Or the ventricle is contracting harder

SOFT S-2 One of the two valves that contribute to

this sound is NOT closing AORTIC REGUGITATION PULMONARY REGURGITATION OR the valve is not present

AORTIC ATRESIA PULMONARY ATRESIA

BOTH ARE CYANOTIC

LOUD S-2 Either one of the valves is stiff and

BANGS shut when it tries to open

AORTIC STENOSIS PULMONARY STENOSIS Or there is HIGH pressure in front of the

valves (systemic or pulmonary hypertension)

S-3 Sound made by a noncompliant ventricle ????????????????

S-3 VOLUME overload DILATED ventricle DECOMPENSATION

S-3 said to be normal ONLY in an adolescent female

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ESTROGEN CONNECTION Estrogen is a muscle relaxant Causes liver to produce many proteins

High ESR or CRP Lipoproteins TBG Angiotensinogen Clotting factors

Especially fibrinogen, but not factor 11

S-4 Sound made by an atrial kick

PRESSURE overload HYPERTROPHY COMPENSATION

Most common gallop (atherosclerosis)

MURMURS! MURMURS! MURMURS! MURMURS CAUSED BY TERBULENCE Reynolds number > 2500

Murmur: if it is in the heart Bruit: if it is in a vessel

Occurs when you have 70% stenosis

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MURMUR GRADES Grade 1: barely audible Grade 2: easily audible Grade 3: pretty loud Grade 4: palpable thrill Grade 5: able to hear with stethoscope off

the chest Grade 6: able to hear across the room

without stethoscope

A SYSTOLIC MURMUR Valves that are supposed to be open are

stenotic ( PULMONARY or AORTIC STENOSIS)

OR valves that should be closed are not closing ( MITRAL REGURGITATION or TRICUSPID REGURGITATION)

SYSTOLIC MURMURS Aortic stenosis Pulmonary stenosis Mitral regurgitation Tricuspid regurgitation Ventricular septal defect

HOLOSYSTOLIC ( PANSYSTOLIC) MURMURS

Tricuspid regurgitation Mitral regurgitation VSD

PANSYSTOLIC increases on INSPIRATION

Tricuspid regurgitation

PANSYSTOLIC increases on EXPIRATION

Mitral regurgitation VSD

Radiates into the axilla: MITRAL

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SYSTOLIC EJECTION MURMURS Aortic stenosis Pulmonary stenosis

AORTIC STENOSIS Radiates to the carotids( neck) LOUDER with leaning forward, making a

fist, blowing up a blood pressure cuff, or squatting

Crescendo decrescendo or diamond shaped murmur

PULSUS TARDUS DELAYED CAROTID UPSTROKE

IHSS Autosomal dominant Muscle fibers are hypertrophied but

disorganized Any young athlete who dies suddenly,

especially during peak exercise Septum is asymmetrically thick, especially

the top > causes SUBAORTIC stenosis

IHSS, cont Excessive hypertrophy compresses the

coronary arteries Excessive hypertrophy obliterates the

ventricular space

Murmur is LOUDER with standing or with Valsalva; decreased with increased TPR

PULSUS BISFERIENS

IHSS, cont Tx: need to decrease contractility; allow

time for adequate ventricular filling Beta blockers Adequate fluid intake Bar from organized sports Do an ECHO on entire family

DIASTOLIC MURMURS Either the valves that should be open are

stenotic (MITRAL STENOSIS or TRICUSPID STENOSIS)

Or the valves that should be closed are regurgitant ( AORTIC REGURGITATION or PULMONARY REGURGITATION)

129129

DIASTOLIC BLOWINNG or DECRESCENDO MURMUR

AORTIC REGURGITATION PULMONARY REGURGITATION

Increases on inspiration: Pulmonary regurgitation

Increases on expiration: Aortic regurgitation

Aortic RegurgitationRadiates to carotids; LOUDER with leaning

forward, making a fist, blowing up a blood pressure cuff, or squatting

Austin-Flint murmur: mitral regurgitationWidens the pulse pressure

bounding pulseswaterhammer pulsehead-bobbingQuinckes pulses

Pulmonary Regurgitation Radiates to the back Louder on inspiration Graham-Steele murmur: tricuspid

regurgitation

Diastolic Rumbles TRICUSPID STENOSIS MITRAL STENOSIS

Increases on inspiration: tricuspid regurgitation

Increases on expiration: mitral regurgitation

CARDIAC PATHOLOGY CARDIOMYOPATHIES DILATED HYPERTROPHIC RESTRICTIVE

CVD Amyloidosis Hemochromatosis

CONSTRICTIVE Tamponade ( Kussmaul sign; Pulsus Parodoxicus)

Trauma cancer

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EFFUSIONS Transudate: mostly water Exudate: mostly protein

Transudate: sp. G < 1.012 Protein < 2grams

Exudate: sp. G > 1.012 Protein > 2grams

Congenital Heart Diseases VSD ASD PDA Coarctation

Cyanotic Congenital Heart Disease Transposition of Great Arteries Tetrology of Falot Tricuspid Atresia Total Anomalous Pulmonary Venous Return Truncus arteriosus Pulmonary Atresia Aortic Atresia Hypoplastic Left Heart Ebstiens Anomaly

VALVULAR DISEASES: most common causes

Aortic stenosis: aging Aortic regurgitation: aging Mitral stenosis: Rheumatic fever Mitral regurgitation: MVP, SBE, collagen

diseases Tricuspid stenosis: Rheumatic fever,

carcinoid syndrome Tricuspid regurgitation: acute endocarditis

Pulmonary Disease Most common cause is ALWAYS

congenital Pulmonary valve is protected on BOTH

sides

131131

Flow Volume Loops

Antiarrhythmics

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Na Channel Blockers Class Ia

Quinidine Procainamide Disepyramide

Class Ib Lidocaine Tocainide Mixeletine Phenytoin

Class Ic Encainide Flecainide Propofenone

Wolf-Parkinson-White Syndrome

Class IV Ca Channel Blockers Verapamil Diltiazem Nefedipine Nicardipine Nimodipine Amlodipine Femlodipine

Class II Beta Blockers End in lol Specific B-1: begin with A thru M (not L,C) Specific B-2: begin with N thru Z (incl L,C)

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Class II Beta Blockers Propanolol Acebutalol Esmalol Atenalol Timolol Pindalol Butexalol Sotalol Labetalol Carvidalol

Class III: K channel Blockers Napa Sotalol Bretylium Amiodorone

THE END

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1

PHYSIOLOGYMidgut (rotation 270)

Foregut (rotation 90)Celiac artery Parasympathetic: Vagus

Sympathetic:splanchnic nerves T5-T9

Hindgut ( Septation)Inferior mesenteric Parasympathetic: pelvic splanchnic nerves

Sympathetic: lumbar splanchnic nerves: L1-L2

Superior mesenteric Parasympathetic: VagusSympathetic: splanchnic

nerves T9-T12

` Gives rise to the GI, from mouth to secondpart of duodenum, including the respiratory tract

` Lungs and upper GI have many congenital connections

` Extends from the second part of duodenum to the spleenic flexure

` Develops in the YOLK SAC

` Must go through a 270 degree rotation as it migrates from yolk sac into abdominal cavity

` MIDGUT ROTATION requires ciliary action KARTAGENERS: SITUS INVERSUS

` FROM splenic flexure to the anus

` WATERSHED AREA: the spleenic flexure H th l t bl d l Has the least blood supply

Most susceptible to ischemic infarcts

`CNSÒRAL`PHARYNGEAL`PHARYNGEALÈSOPHAGEALÙGI`LGI

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4/29/2008

2

` SENSORY INFORMATION THINKING about food HEARING about food SMELLING food TOUCHING food TASTING foodTASTING food

ALL sensory information must reach the cortex; Response is via the CORTOCOBULBAR pathway via the vagus No longer do a vagotomy for peptic ulcer disease (cant enjoy

food) Highly selective parietal cell vagotomy now

` Cortex can over ride any basic urge:(outer layer of the cerebrum-forgut)

` LIMBIC SYSTEM- responsible for basic urges Hippocampus long term memory Amygdala- reward and fear, mating

Responsible for setting time: Circadian rhythms

` Neurotransmitter: melatoninLight outside- melatonin low- DAYTIMEDark outside melatonin high NIGHTDark outside- melatonin high- NIGHT

Morning- catabolic processes are in their highest function- working out in the morning is the best

Melatonin from tryptophan- milk and turkey

- Bright lights in companies, casinos

- 1st, 2nd, 3rd shift workers/ workers comp

Feeding Center(HUNGER)

` Location: Lateral hypothalamus

Satiety Center

` Location: Vento-medial nucleus of

the hypothalamus

Destruction: AnorexiaDestruction: Hypothalamic obesity syndrome

Lateral hypothalamus

` Stimulus: Feeding (hunger) Glucose

If

pass program

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