path/pharm summaries ms/gi/heme/renal

8/6/2019 Path/Pharm Summaries MS/GI/Heme/Renal

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Synopsis of Anatomy / Physiology / Pathophysiology / Pharmacology

Arranged by body system:

Dr. Kelner

Gastrointestinal Pathophysiology and Pharmacology

I. Basic anatomical and physiologic concepts

A. Gross Anatomy and Physiology

1. The GI tract consists of a long tube (the alimentary canal) that extends from

the mouth to the anus.

2. There are accessory organs that connect to this tube along the way

a. Liver

i) Responsible for initial metabolism of nutrients and drugs

ii) Receives blood supply from gut via the large portal veiniii) After processing is done, the blood leaves the liver via the hepatic

vein and empties into the inferior vena cava

iv) The liver also produces Bile necessary for the emulsification of lipids

v) The liver is the site of production of many proteins including albumin

and clotting factors

b. Gallbladder (GB)

i) located below and somewhat behind the liver

ii) stores bile that is initially produced in the liver

iii) bile exits the gallbladder via the cystic ductthis joins with a

similar structure leaving the liver called the hepatic ductaftercoming together.they form a singular common bile duct (CBD)

c. Pancreas

i) the pancreas is both an endocrine and exocrine organ. The endocrine

function involves the secretion of insulin and glucagon into the vascular

system. The exocrine function involves the secretion of digestive

enzymes and bicarbonate into the duodenum.

ii) the pancreatic duct and the CBD empty into the duodenum via

the ampulla of vater

iii) pancreatic enzymes consist of peptidases (catabolize proteins),

amylase (catabolizes carbohydrates), lipase (lipids) and nuclease

(nucleic acids). Note that the amylase produced by the pancreas is

not exactly similar to that produced by the salivary glands

iv) HCO3- (bicarb) is secreted into the proximal duodenum in

response to Secretin. This hormone is released by the duodenum

in the presence of low pH

v) The duodenum also releases cholecystokinin (CCK) in response


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to the presence of lipids. The release of CCK stimulates the GB

to release bile into the duodenum.

3. The alimentary canal follows this path:

epiglottis hiatus/ GES pyloris

Mouth Pharynx Esophagus Stomach duodenum ileocecal valve hepatic flexure

Jejunum Ileum Cecum ascending colon transverse

splenic flexure

colon descending colon sigmoid rectum anus Vol. and invol.

sphincters

B. Digestive physiology and histology

1. Chemical digestion begins in the mouth where the salivary glands release

amylase

2. The process of swallowing is called Deglutination

3. The epiglottis closes off the opening of the trachea during deglutination.

Problems with this process lead to aspiration. Remember that the Gag reflex

is controlled primarily by the ninth cranial nerve (Glossopharyngeal).

4. The bolus of food swallowed is pushed along the esophagus by peristalsis.

Remember that there are muscles that are arranged both longitudinally along

the esophagus and also circumferentially

5. The esophagus travels through the diaphragm in an opening called theesophageal hiatus. The gastroesophageal sphincter (GES) connects the

esophagus to the stomach and prevents retrograde flow during contraction

of the stomach. If incompetent, it allows such retrograde flow up into the

esophagus which is termed reflux.

6. In the stomach, both chemical and mechanical digestion occurs.

a. the parietal cells lining the stomach produce hydrogen ions (protons)

which are secreted into the lumen of the stomach. Here they join Cl-

and form HCl. The chemical apparatus in the parietal cell that generates

the protons is called the proton pump.

b. Acid production and secretion are increased in response to:

stimulation of H2 receptors on the stomach the presence of protein in the stomach gastrin release (by the chief cells in the stomach)


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c. The stomach is protected from its own acid by a protective layer of

mucus that coats the stomach wall. The production of this mucus is

dependent on the production of certain prostaglandins by an enzyme

called cyclo-oxygenase I (COX I). Inhibition of this enzyme by non-

specific NSAIDs is what leads to NSAID related gastritis and PUD.

d. Minimal absorption does occur in the stomach. Substances known to

be absorbed here include H2O, ASA and ETOH

e. The chyme (partially digested food) exits the stomach through the pyloric

valve. Rarely, this valve is congenitally stenotic (mostly in males) and leads

to dysphagia and projectile vomiting early in life. This is called Pyloric

stenosis and needs to be corrected surgically. This usually occurs at about

six to eight weeks of age.

7. The duodenum is adherent to the posterior peritoneal wall via ligaments

and other connective tissue.

8. The mucosal lining of the GI tract mostly consists of ciliated columnarepithelium. The mucosa forms outcroppings called Villi which serve to

increase the absorptive surface area.

**For further anatomical and physiologic information, see my notes and/or the text**

II. Pathophysiology and pharmacology highlights

A. Gastro-intestinal bleeding (GIBs)

1. GIBs are somewhat arbitrarily defined as upper GIBs and lower GIBs. The

anatomic structure that defines upper from lower is the ligament of Trietz (one

of the structures that holds the duodenum to the back wall). This is locatedabout halfway down the duodenum.

2. Upper GIBs are usually the result of PUD, gastritis, esophageal varicies or

malignancy.

a. the TYPICAL upper GIB is characterized by the presence of melena (dark

tarry stools). This occurs because blood that leaks into the stomach is

acted upon by pepsin (a peptidase) found in the stomach. This catabolism

results in the formation of pigmented by-products(from catabolism of HgB).

Other findings include the possibility of hematemesis, elevated serum BUN

(from the previously mentioned digestion).

b. if the bleeding is OCCULT (slow enough to occur for some time without

being noted), the patient will become anemic and develop fatigue and SOB.

c. Rapid acute upper GIBs will lead to hematochezia (bright red or burgundy

rectal bleeding) as the blood travels down the GI tract too fast to be

catabolized.


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3. Lower GIBs are usually the result of diverticular disease, internal or external

hemorrhoids, polyps or malignancy.

a. typical lower GIBs are characterized by hematochezia

b. similarly to OCCULT upper GIBs, lower GIBs that are occult will lead to

symptomatic anemia

4. Most complete physical exams include a rectal exam. As part of this exam,

the examiner should test stool for the presence of blood. This is called a

Guaiac test and the brand name is frequently called hemoccult.

B. Obstruction

1. Obstructive processes are divided into simple (actual mechanical obstruction)

and functional (physiologic cessation of peristalsis). The functional type is

called an ileus, or sometimes a paralytic ileus. It is more common then the

simple type. An ileus frequently occurs after intra-peritoneal surgery, with

chronic illness or severe acute illness.2. Obstruction is usually heralded by abdominal pain and distention, minimal

(if any) bowel sounds, lack of rectal output and occasionally emesis.

3. Simple mechanical obstructions frequently require surgical repair.

4. An ileus is usually treated with initial decompression of the GI tract using

an Ng tube hooked up to suction, then slowly advancing a PO diet (starting

with clear liquids).

5. If unable to advance diet, the patient may require temporary TPN (total

parenteral nutrition) .feeding the patient intravenously. This situation

is not beneficial if it lasts for weeks. If a patient requires TPN, most

hospitals have a TPN team or nurse that coordinates this therapy. Surgicalplacement of a large bore central venous catheter is required.

6. Acute absence of bowel sounds in a patient who previously demonstrated

them and/or has no obvious reason for an ileus to occur is considered a

SURGICAL EMERGENCY. Delay of acute treatment in this situation can

lead to perforation or rupture of the GI tract.which usually results in

significant morbidity or death.

C. Peptic ulcer disease (PUD)

1. PUD is a characterized by a spectrum of abnormalities, ranging from irritation

of the stomach or duodenal mucosa with minimal inflammation to erosion /

ulceration of the mucosa with perforation.

2. PUD occurs due to:

an increase in acid secretion a decrease in production or maintenance of protective mucus a combination of these two factors

3. Risk factors are delineated in the power point notes


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4. Most cases of persistent or chronic PUD are associated with the presence of

a gram negative bacteria called helicobacter pylori (H. Pylori)

a. definitive treatment therefore consists of anti ulcer medications plus a

regimen of antibiotics

b. diagnosis of H pylori involves biopsy and culture (best way) or a breath

test that checks for the presence of hydrogen sulfide gas. This is produced

by bacterial metabolism of urea by an enzyme called urease

5. Treatment of PUD involves modification of risk factors and pharmacologic

therapy. This section is from the GI power point handout (note: there are a

few changes which are highlighted):

PUD Treatment Classes of anti-ulcer drugs

Antibiotics

Anti-secretory agents Histamine 2 Receptor antagonists Proton pump inhibitors

Mucosal protectantsAntacids

PUD Treatment Histamine (H2) Blockers

Inhibit gastric acid secretion by completely blocking H2 receptor

on parietal cells Suppress nocturnal and Basal gastric acid secretion by 90-95%

and meal stimulated acid secretion by 70-80% Indirectly inhibits pepsin activityAll four H2 Blockers are equally effective when taken in

equipotent doses

H2 BlockersCimetidine (Tagamet)Ranitidine (Zantac)Famotidine (Pepcid)Nizatidine (Axid)PUD Treatment


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H2 Blockers Ranitidine (Zantac)

Cimetidine (Tagamet) - PROTOTYPE Famotidine (Pepcid) Nizatidine (Axid)All H2 receptor blockers require a dosage reduction in

patients with significantly decreased renal or hepaticfunction

PUD TreatmentH2 Blockers (cont.)

ActionsPharmacokineticsAdverse effectsDrug interactionsTherapeutic uses

Gastric and duodenal ulcers

Gastroesophageal reflux disease

Zollinger-Ellison syndromeAspiration pneumonitis

Heartburn, acid indigestion, and sour stomach

Preparations, dosage, and administration

H2 Blockers Actionssuppress secretion of HCl by parietal cells of

stomachcan be give orally or intravenouslybind to androgen receptors resulting in reversible

gynecomastia, reduced libido and impotenceH2 Blockers Drug Interactionsreduces the activity of hepatic cytochrome P450 --

the family of drug metabolizing enzymes


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particular concern w/ warfarin, phenytoin,theophylline & lidocaine

antacids decrease absorption w/ po

more problems w/ cimetidinePUD Treatment Cimetidine (MOST SIDE EFFECTS)

Many drug interactionsAnti-androgenic effects with cimetidine

Gynecomastia, reduced libido, impotence CNS effects with cimetidine

Confusion, hallucinations, lethargy, restlessness

PUD TreatmentThere are two mechanisms to decrease the amountof HCl secreted in the stomachdecrease the amount of HCl secreted by the

parietal cells of the stomach (using H2 blockers)decrease the amount of HCl produced &

therefore availablePROTON PUMP INHIBITORS Drug of choice for hypersecretory conditions Rapid healing of erosive esophagitis and refractory

Adverse effects: Headache, nausea, abdominal pain,vomiting, dyspepsia, flatulence

PUD Treatment Proton pump inhibitors (PPI):

Omeprazole (Prilosec) most effective Lansoprazole (Prevacid) Esomeprazole (Nexium)

Inhibit activity of the proton pump in the parietal cellsActivation of proton pump is final step in acid secretionAbolishes gastric acid secretion in response to any type of stimulus

PUD Treatment


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Omeprazole (Prilosec) most effective Minimal side effects with short-term therapy; with long-term,

concern about possible carcinogenesis Mechanism of action

Pharmacokinetics

Therapeutic useAdverse effects

Preparations, dosage, and administration

Other PUD Drugs Mucosal defense agents

Binds selectively to ulcerated mucosa and forms a barrier Protects ulcer from gastric acid and pepsinAllows ulcer to heal from within

Bismuth (Pepto-Bismol) Sucralate (Carafate)

MUCOSAL DEFENSE ENHANCERSSucralfate (Carafate)

Binds selectively to ulcerated mucosa and forms a barrierProtects ulcer from acid and pepsinAllows ulcer to heal from withinAdverse effects: constipationSeparate doses of this and antacids by 2 hrs

Other PUD Drugs

Sucralfate (Carafate)Effective with minimal side effects and lack of significant drug interactions

Mechanism of action Pharmacokinetics Therapeutic usesAdverse effects Drug interactions Preparations, dosage, and administration

Note: Pepto-bismol is a bismuth based agent that acts to assist the mucus layer

protection of the stomach. Using this drug will lead to darkening of the stoolswhich can mimic melena. Bismuth also shows up on x-ray. The agent

misoprostol (Cytotec) is rarely used any more because of adverse effects. It is a

prostaglandin type agent that contributes to the mucus protection. This chart

shows OTC meds available for PUD treatment including the neutralizing

antacids:


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D. Inflammatory Bowel Disease1. Consists of Ulcerative Colitis and Crohns disease

2. There are many similarities between these two disorders and also a fewimportant differences. The following chart is helpful in delineating these

differences

Comparison of Ulcerative Colitis and Crohn's Disease

Feature Ulcerative Colitis Crohn's Disease

Distribution Diffuse, distal predominanceSegmental or diffuse, often proximalpredominance ILEAL INVOLVEMENT

Rectum Always involved Often spared

Microscopic Distribution Diffuse Often focal

Depth of Inflammation Mucosal Transmural

Sinus Tracts and Fistulae Absent Often present

Strictures Absent Often present

Granulomas

COMPLICATIONS

Absent

Toxic Megacolon

Often present

FISTULA FORMATION


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Ulcerative Colitis Crohns Disease

Information regarding the etiology of IBD:

The causes of ulcerative colitis and Crohn's disease are not known. However, a reasonable hypothesis for

the pathogenesis of inflammatory bowel disease can be presented. As yet unidentified antigens, possibly a

mycobacterium, paramyxovirus, or components of cigarette smoke, activate resting macrophages to release

a wide variety of cytokines.3Cytokines is a collective term for a group of low-molecular-weight peptides

that are active at low concentrations and bind to specific receptors to produce autocrine, paracrine, and

endocrine effects. The most abundant cytokine is interleukin-1 (IL-1), which not only causes diarrhea but

also acts as a pyrogen. Other cytokines activated in the inflammatory process are IL-6, tumor necrosis

factor a (TNF-), and the chemokine IL-8. Cytokines cause differentiation of lymphocytes to different

types of T cells. Helper T cells, type 1 (Th-1), are associated principally with Crohn's disease, whereas Th-

2 cells are associated principally with ulcerative colitis. These cytokines serve to stimulate the immune

system and cause an inflammatory reaction, thus producing tissue damage in the intestinal mucosa.

This is a summary from this URL:

http://www.clevelandclinicmeded.com/medicalpubs/diseasemanagement/gastroenterology/inflammatory-bowel-disease/

Summary

Ulcerative colitis is characterized by mucosal inflammation of the colon, whereas Crohn's

disease is characterized by transmural inflammation involving any part of the

gastrointestinal tract.

The diagnosis of ulcerative colitis or Crohn's disease is based on a constellation of

positive endoscopic, radiographic, and histologic findings, with negative stool cultures.

The differential diagnosis of irritable bowel syndrome includes infectious colitis, celiac

sprue, intestinal lymphoma, radiation enteropathy, NSAID use, and ischemic colitis.

First-line therapy for ulcerative colitis patients includes 5-aminosalicylic agents, and

some patients also may need corticosteroids, immunosuppressives, and biologic agents.

First-line therapy for Crohn's disease patients often includes budesonide, and some

patients also may need other corticosteroids agents, immunosuppressives, antibiotics, and

biologic agents.

Colorectal cancer risk is an important concern for patients with ulcerative colitis or

Crohn's colitis.


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The 5-aminosalicylic agents include: Oral Aminosalicylates Sulfasalazine (Azulfidine)Rectal Aminosalicylates MesalamineThese agents are actually useful in both Crohns and UC. The treatment approach for IBD

is a stepped approach and is well documented in this image:

E. Portal Hypertension the sections in the GI DISORDERS handout regardingPortal HTN / Ascites / Hepatic Encephalopathy / Jaundice are concise and outlinethe material well. I will not redo that here.

F. Viral hepatitis

1. There are many types of viral hepatitis. They are pretty much all categorized

by marked elevation of the liver enzymes (AST and ALT) and bilirubin levels.

Most hospitals have a lab panel called a liver or hepatic profile that consists of

these measurements. The panels may also include a few other values like

Alkaline phosphatase and GGT (gamma-glutamyl transferase). Elevation of

these substances can also occur in viral hepatitis, but can also occur in anumber of other conditions.

2. For our purposes, we will focus on types A, B and C.

a. Type A is mostly transmitted by the food borne route (ie. fecal-

oral transmission). In almost all cases, Hep A is self limiting (goes

away on its own with supportive treatment) and does NOT result in

Chronic hepatitis. Outbreaks of this type of hepatitis frequently

occur secondary to tainted food supplies and/or poor hygiene by

food service workers.

b. We will look at types B and C together. there are a few differences,

but for the most part they have similar courses. These types of viral

hepatitis are primarily transmitted venereally (through body fluids).

These types of viral hepatitis are associated with promiscuity, un-

protected sex and IV drug use. They can also be transmitted via

poorly screened blood that is transfused. Both type B and C can

lead to Chronic hepatitis with subsequent hepatic failure. Liver


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cancer risk is also markedly increased in patients with types B/C.

Most hospitals have a Viral Hepatitis Profile which is used to

characterize the specific type of viral hepatitis that is present in a

given patient. It should be noted that IgG antibodies, when present

alone, do not signify acute disease. The presence of IgG antibodies,

in the absence of other types, usually signifies past disease or HEP B

vaccination. The presence of IgM antibodies along with other specific

antibodies signifies acute disease. Treatment for chronic viral hepatitis

involves immune suppressive therapy and Interferon alpha. Interferon

is a type of cytokine released from lymphocytes that has anti-viral

properties. It is given parenterally, very expensive and frequently

causes severe flu-like adverse effects. Patients often become non-

compliant due to these factors. The most aggressive form of therapy is

liver transplant. This surgery is plagued with many issues. The patients

who are to be considered must demonstrate documented sobriety for atleast six months and usually a year. After successful documentation is

received, the patient is then out on the transplant list. The waiting

period is often lengthy and the patient frequently worsens during this

period and/or relapses on alcohol and/or drugs.

The above information regarding viral hepatitis is sufficient, the other information in thepower point outline can be ignored for now.

Regarding Cirrhosis, alcoholic cirrhosis, cholelithiasis, cholecystitis and pancreatitis

(acute), the information in the outline does not need to be repeated here. I will list a fewimportant points however:

1. On physical exam, the patient with cirrhosis will have a very small NON-

PALPABLE liver.

2. Remember that patients with end stage liver disease have clotting issues (elevatedPT/INR) due to insufficient production of clotting proteins. They will also be

globally edematous secondary to markedly decreased oncotic pressure. Thisoccurs secondary to inability of the diseased liver to produce albumin.

3. Almost all gallstones are made of precipitated and crystallized cholesterol.

4. Remember that these patients often demonstrate an exacerbation of their symptoms

after a meal containing lipids. They may also have right scapular pain that is referred.Treatment is almost always laparoscopic cholecystectomy.

5. Acute pancreatitis is most commonly due to alcoholism or cholelithiasis. It

presents as severe mid-epigastric pain often associated with vomiting. Diagnosisis usually made when a patient presents with the previously discussed risk factors


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and symptoms combined with elevated serum Lipase and Amylase. Treatmentinvolves gut rest usually maintained with an Ng tube hooked up to suction,

followed by a slow advancement of their diet. Recurrent acute pancreatitis canresult in chronic pancreatitis, which is associated with significant morbidity and

mortality.

Regarding the anti-emetic drugs, refer to this list :

Promethazine (Phenergan)Promethazine is also known as phenergan and mepergan. It is also used to treat motion

sickness, reduce allergic symptoms, and forsedation. It is one of the drugs of thephenothiazine type. In addition to other qualities, it is an antihistamine. Promethazine is

given in doses of 12.5 to 25 mg every 4 hours if injected into the muscle or as asuppository. As a syrup, 25 mg should be given every 4 to 6 hours. Doses for children

vary by age, weight, and severity of condition. Patients taking promethazine may

experience a large number of side effects, including drowsiness, ringing in the ears, alack of coordination, problems with vision, fatigue, euphoria, nervousness, tremors,seizures, a catatonic-like state, and hysteria. These effects are usually reversible. At high

doses, patients may also exhibit extrapyramidal reactions. Extrapyramidal reactions canbriefly be described as agitation (jitteriness, sometimes insomnia), muscle spasms, and/or

pseudo-Parkinson's (a group of symptoms including, but not limited to, drooling, tremors,and a shuffling gait).

Prochlorperazine (Compazine)Prochlorperazine is also known as compazine. Like promethazine, it is a member of theclass of phenothiazines. Unlike promethazine, however, prochlorperazine also belongs to

the class of drugs known as antipsychotics, or neuroleptics. Antipsychotic drugs are usedto treatpsychoses and other psychiatric disorders. In addition to its use as an antiemetic

and anti-psychotic drug, prochlorperazine is also used to treat non-psychotic anxiety.Generally, the dose is 5 to 10 mg, 3 to 4 times per day. However, the effect of medication

varies widely from patient to patient, so the dose should be tailored to each individual.Prochlorperazine is available as a syrup, tablet, 25 mg slow-release capsule, and in

injectable form. Prochlorperazine has many side effects, including low blood pressure,dizziness,blurred vision, skin reactions, and jaundice. Two other (rare) disorders, tardive

dyskinesia and neuroleptic malignant syndrome (NMS), are also associated withantipsychotic drug use.

Serotonin Receptor Antagonists

The serotonin receptor antagonists include granisetron (kytril), dolasetron (anzemet), and

ondansetron (zofran). These drugs are used for postoperative nausea and emesis as wellas nausea and vomiting associated with chemotherapy, and are often used in combination

with a corticosteroid. Ondansetron is approved for nausea and vomiting associated withradiation therapy. The use of these agents in the treatment of nausea not associated with

surgery and/or chemotherapy is becoming more common. These agents antagonizeserotonin receptors directly within the hypothalamic emesis center. They are often


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effective in cases where phenergan and/or compazine are not effective. The majordrawback of these agents is cost.

The primary information that I want you to be aware of concerning the anti-emetics is the

category of drug (eg. phenothiazine), primary adverse effects and the fact that phenerganand compazine are much lower in cost compared to Zofran and other serotonin drugs.

Laxatives regarding the laxatives, know the four primary types, how they work and an

example of each. This information is found in the GI outline and can be furtherreinforced here:

http://en.wikipedia.org/wiki/Laxative

Anti-diarrheal agents both agents that are commonly used to control diarrhea are

opiate derivatives. Remember that opiate pain medications generally have constipationas a side effect. The two agents are Diphenoxylate (Lomotil) and Loperamide

(Imodium). For some reason, these are listed in the outline as non-opioids.but that isnot accurate. These agents will sometimes lead to positive results for opiates on a drug

screen.

Musculoskeletal / Rheumatologic Pathophysiology and Pharmacology

Notes on normal anatomy and physiology:

1. Remember that bone is in general a very vascular and metabolically active tissue.

It serves as a repository for calcium and phosphorus. Osteocytes are mature bonecells. Osteoblasts build bone, and osteoclasts break it down.

2. Long bones (such as the femur) have three main sections. The ends of the bone

are lined with articular cartilage and are called the epiphysis. The shaft is called

the diaphysis and between those two sections, one finds the metaphysis, alsoknown as the growth plates. By the time one reaches their early twenties (orbefore), the metaphyseal regions are completely calcified.

3. Most joints in the body fall into one of two categories. Either they are

non-synovial (like the skull joints) or synovial (knees, hips, elbows, fingers,etc). The synovial joints are characterized by the presence of synovial

capsules surrounding the joint and containing synovial fluid. This fluidacts as lubrication.


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These joints are more flexible then non-synovial joints and provide moreprotection and cushion then non-synovial joints. The downside is that the

synovial tissue is the tissue attacked in patients with rheumatoid arthritis.

4. Healing bone (after a fracture) forms a CALLUS around the fracture site. Thisis the only term that you need to understand from this page.

5. Remember that muscle tissue contracts secondary to actin sliding over myosin.

It takes energy, in the form of ATP, to relax after contraction. This is whypatients who expire have a period of Rigor Mortis. No lifeno ATP..no

muscle relaxation. Also, muscle uses creatinine phosphate as an energy carrier,in addition to ATP.

FRACTURES

A fracture is another term for a broken bone. There is NO difference between a fracture

and a break. Some fractures are COMPLETE meaning that extend through the cortex on

both sides of the diaphysis.some fractures are termed GREENSTICK FRACTURES,

meaning that they extend through only one side of the cortex (similar to trying to break a

branch of a tree that is still living). Another term(s) that describes the character of a

fracture is simple (closed) orcompound (open). Fractures that are termed open are

exposed to the outside world through a break in the skin surface. An open fracture is

considered an orthopedic emergency. They absolutely need to be evaluated by an

orthopedic surgeon. Most of the time, these patients will go to the OR to have the

fracture site cleaned and repaired. Obviously the biggest risk in this situation is infection.

In the evaluation of ANY extremity injury (fracture, dislocation, laceration, etc...), THE

FIRST THING THE NURSE MUST DO IS EVALUATE FOR NEUROVASCULAR

INTEGRITY DISTAL TO THE INJURY. Feel for pulses and make sure that the patient

has intact motor and sensory function. This evaluation is critical as a patient with

impaired neurovascular integrity will require IMMEDIATE intervention. This evaluation


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will also most likely be ordered every few hours after the injury is repaired. Again, if the

limb was neurovascularly intact after repair of the injury and now is not....This requires

IMMEDIATE evaluation. Damage to the nerve and/or limb ischemia can lead to

permanent disability if not recognized and treated immediately.

Regarding the types of fractures, here are a few notes in addition to the information foundon the power point outline (which is also up on sonis).

1. As noted, a COMMINUTED fracture means that there are MORE THEN TWO bone

fragments. When somebody says, I shattered my ankle...this is what they mean.

Here are some images of different types of fractures:

2. A torus fracture., also called a buckle fracture is seen primarily in children. Thecortex of their bone is not fully calcified and therefore it is soewhat elastic in nature.When a fracture occurs, the cortex buckles out instead of completely fracturing into two

fragments.

Here is an image of TORUS fracture of the radius:


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Sometimes, you can not even make out the fracture line, you only see evidence of abuckle as you follow the cortex. These can missed easily if you do not know what to

look for.

I should also note here that when evaluate bony injuries in children, it can be verydifficult to tell the difference between a fracture and an incompletely ossified metaphysis.

One trick is to order the same x-ray view of the unaffected limb and compare them. Ifyou see additional lines on one side...it is probably a fracture. This is a NORMAL x-ray

of a childs elbow:


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You can see how difficult it might be to differentiate a fracture from a normal non-ossified growth plate.

3. Spiral fractures require a twisting mechanism of injury to occur. If one notes a spiral

fracture in a child with a history not consistent with a twisting motion, for example, if the

parents state that the child fell off the couch, and there x-ray looks like this:

It is considered CHILD ABUSE...until proven otherwise. All suspected abuse HAS TO

BE EVALUATED. Children services will usually be called. This is a very difficultsituation, especially if there is no abuse....but more often then not....a spiral fracture

accompanied by a history not consistent with a twisting motion....means abuse!

This image shows the different types of fractures very well:

4. A PATHOLOGIC fracture means that a fracture occurs without an appropriate

amount of force to produce such fracture. In other words, the fracture would not


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have occured if there was not underlying bone disease (eg. osteoporosis, bonytumor,etc...). When you here of an elderly lady who broke her hip by just gettingout of bed...this implies a pathologic fracture. One can see a fracture in the mid-tibia here. There is an underlying tumor, which weakened the bone and made itpossible for a fracture to occur without the force that would be required if the

bone was not diseased:

5. A STRESS fracture is often very subtle and occurs due to repeated stress at a

specific anatomic location. For example, an athlete who is training for amarathon and runs several miles per day on hard surface may suffer a streesfracture to one of the metatarsals:

Many times the only way to diagnose a stress fracture is to obtain a nuclear bonescan. In this test, the patient is injected with nuclear contrast material that will


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show up under a nuclear camera. It will LIGHT UP in areas where there isincreased metabolic activity like a healing fracture or a malignancy. This bonescan shows a stress fracture of the calcaneus that did not show up on plain x-ray:

You can obviously see how the calcaneus lights - up.

Dislocation / Subluxation

The difference between these two terms is that a subluxation implies that thebone that is displaced from the joint is still partially in contact with the joint. A

dislocation implies that there is no contact between the displaced bone and thejoint. In the real world, these terms are often confused and used interchangably.

Many times chiropracters will use the term subluxation to imply that there hasbeen some movement between the articulating surfaces (articulating means thatthey are forming a joint). This may or may not be accurate...and many times theangle that they point out to the patient is perfectly normal....but just looks angled.Like any profession, there are good ones and bad ones....just be careful. This isan x-ray of a complete dislocation of a shoulder:

You can see how the head of the humerus is completely out of the glenoid joint.This is a subluxation of the same joint:


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You can see that is some contact (albeit minimal) between the humerus and thejoint. Remember, as with any limb injury, the first thing that must be done oninitial evaluation of a patient with a suspected dislocation or subluxation, is to

evaluate the limb distal to the injury for neurovascular integrity. If you are theprimary evaluating person, always get an x-ray of a suspected

dislocation/subluxation, even if the patient states that this has happened manytimes before, becuase occasionally a fracture can occur ALONG WITH adislocation. If you try to reduce the dislocation (put it back into place) and thereis an associated fracture...you can cause permenant damage.

Also, I should state here, that the term REDUCTION implies either putting adislocated bone back into the joint or aligning the fragments of a fractured bonebefore casting it. In regards to the fracture, the reduction can either be describedas an open reduction or a closed reduction. The difference is that in an open

reduction, the patient is taken to the operating room and surgical reduction isrequired (usually with the placement of pins or a plate or wire to hold it in place).Most fracture reduction are of the closed type and are done without surgery,although conscious sedation may be required. When you look at the chart ofmany nursing home residents, especially females, you will see this as part ofthere history: ORIF right or left hip. This is an abbreviation for Open Reductionwith Internal Fixation and is very common in patients who have had a hip

fracture.

Sprains and Strains

There is technically a difference between these terms, but in the real world theyare used interchangably. Therefore, you do not need to differentiate betweenthem. You should, however, know the difference between a ligament and atendon. Often, a severe sprain can more difficult to heal then a fracture. For


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example, the ligaments on the outside of the ankle, called the deltoid ligaments,are so strong, that when the ankle is inverted (twisted with the plantar surface ofthe foot pointing medially), the distal part of the tibia is avulsed (torn away) ratherthen the ligament tearing. In this x-ray, you can see that the tip of the tibia isavulsed from the shaft:

The treatment of sprains and strains can be summarized by the word RICE(REST, ICE, COMPRESSION and ELEVATION). Most of the time, we do notrest the injury long enough and it remains unstable for life....and will become

sprained even with minimal force. Remember also, that NSAIDs are very helpful

in the treatment of these injuries. One should use them on a scheduled basis for3 - 5 days. This builds up a blood level and will help to relieve the swelling.Using them only PRN for pain does not really acheive this.

OSTEOPOROSIS

This disease of bone mineralization is very common. It occurs much morefrequently in women as they require a certain level of estrogen to mineralize theirbones. This is a good basic summary of osteoporosis:

Osteoporosis, which means "porous bones," causes bones to become

weak and brittle so brittle that even mild stresses like bending over,lifting a vacuum cleaner or coughing can cause a fracture. In most

cases, bones weaken when you have low levels of calcium, phosphorus

and other minerals in your bones.


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A common result of osteoporosis is fractures most of them in the

spine, hip or wrist. Although it's often thought of as a women's

disease, osteoporosis also affects many men. And aside from people

who have osteoporosis, many more have low bone density.

This is a good summary of causes:

Throughout ones lifetime, old bone is removed (resorption) and new bone is

added to the skeleton (formation). During childhood and teenage years, new

bone is added faster than old bone is removed. As a result, bones become

larger, heavier, and denser. Bone formation outpaces resorption until peak bone

mass (maximum bone density and strength) is reached around age 30. After that

time, bone resorption slowly begins to exceed bone formation.

For women, bone loss is fastest in the first few years after menopause, and it

continues into the postmenopausal years. Osteoporosiswhich mainly affects

women but may also affect menwill develop when bone resorption occurs too

quickly or when replacement occurs too slowly. Osteoporosis is more likely to

develop if you did not reach optimal peak bone mass during your bone-building

years.

RISK FACTORS:

Risk factors you cannot change:

Gender. Your chances of developing osteoporosis are greater if you are a

woman. Women have less bone tissue and lose bone faster than men

because of the changes that happen with menopause.

Age. The older you are, the greater your risk of osteoporosis. Your bones

become thinner and weaker as you age.

Body size. Small, thin-boned women are at greater risk.

Ethnicity. Caucasian and Asian women are at highest risk. African

American and Hispanic women have a lower but significant risk.

Family history. Fracture risk may be due, in part, to heredity. People

whose parents have a history of fractures also seem to have reduced

bone mass and may be at risk for fractures.

Risk factors you can change:


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Sex hormones. Abnormal absence of menstrual periods (amenorrhea),

low estrogen level (menopause), and low testosterone level in men can

bring on osteoporosis.

Anorexia nervosa. Characterized by an irrational fear of weight gain, this

eating disorder increases your risk for osteoporosis.

Calcium and vitamin D intake. A lifetime diet low in calcium and vitamin D

makes you more prone to bone loss.

Medication use. Long-term use of glucocorticoids and some

anticonvulsants can lead to loss of bone density and fractures.

Lifestyle. An inactive lifestyle or extended bed rest tends to weaken

bones.

Cigarette smoking. Smoking is bad for bones as well as the heart and

lungs.

Alcohol intake. Excessive consumption of alcohol increases the risk of

bone loss and fractures.

This Site has an excellent summary...I will not copy it here:

http://www.niams.nih.gov/Health_Info/Bone/Osteoporosis/default.asp

Important:

1. Prevention involves adequate calcium and vitamin D intake,

especially during the pre-menopausal years in women.

2. Pathologic fractures and vertebral compression fractures are very

common in patients with osteoporosis. Multiple vertebral

compression fractures can cause kyphosis (dowagers hump) inwomen and height loss.


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COMPRESSION FRACTURES:

Kyphosis:

3. A bone density test (non-invasive) is used to diagnose osteoporosis:


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This produces a report which compares the patients results to normalized valuesand also, over time, allows one to compare their density with previously donetests.

The most common agents used in the treatment of osteoporosis are shown in the

following table:

How It Works

Bisphosphonates are antiresorptive medicines, which means they slow or

stop the natural process that dissolves bone tissue, resulting in maintained

or increased bone density and strength.1 This may prevent the

development of osteoporosis. If osteoporosis already has developed,

slowing the rate of bone thinning reduces the risk of broken bones.


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Biphosphanates should not be used by non-ambulatory patients. After taking

these medicines, one should move around for awhile to prevent the medication

from being in contact with the same stomach area for an extended period of time

as this can cause erosion and ulcer symptoms.

These medications are also indicated for Pagets disease, which is a disease ofimpaired bone remodeling. It is not very common, but does appear on exams

(not just mine). So remember to associate Pagets disease with the word

remodeling.

This x-ray of the leg bones in a paget with long term Pagets

disease shows obvious problems with bone mineralization andremodeling:

There are currently some new treatments for vertebral compression fractures that

involve the injection of an acrylic like material into the vertebrae to restore height.Pain secondary to the fracture is usually decreased as well.


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Occasionally calcitonin is used to treat osteoporosis.

Osteomyelitis is the term for bone infection and used to be much more commonthen it is now. More soldiers died of this then anything else during the civil war.This pathology is much more common in patients with vascular perfusionimpairment...like those with diabetes. Patients with long term skin and soft tissueinfection can develop osteomyelitis as the infection spreads to the bone. Theseinfections are often very hard to eradicate and usually require at least 6 weeks ofIV antibiotics. This is frequently done at home using a long term central venouscatheter (PIC line) and home health care nurses. Here are a few images of

osteomyelitis:

On bone scan:


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In the OR:

Osteoarthritis

OsteoarthritisAlso called Degenerative joint disease or wear and tear arthritisNoninflammatoryDoes not involve synoviaRisk factors include age , prior trauma and geneticsPrimary defect is loss of articular cartilageSymptoms include pain and stiffnessDiagnosis is made via H+P and xray studies

Treatment includes NSAIDs, Tylenol and surgery

* This type of arthritis is much more common then rheumatoid arthritis* This is the type of arthritis that one gets from chronic strain to aparticular joint.* Remember...it is non-inflammatory....anti-inflammatories may help thepain, but they will not change the course of disease* This is the type of arthritis that one frequently hears the phrase, boneon Bone in the description of the xray findings. This means that thearticular cartilage is completely worn away and the joint space is markedly


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reduced. This finding associated with pain and/or disability usually

precedes joint replacement surgery. This is good xray image:

Rheumatoid Arthritis

Autoimmune destruction of synovial joint structures

Affects all age groups, although in pediatric group, called Juvenile

RA(Stills Disease)

More common in femalesSymptom include:

Joint pain, stiffness and swellingSystemic symptoms such as fever, rash, malaise, Raynauds

phenomenaJoint deformity

Rheumatoid nodules

Treatment includes:RestHot/cold packs

Physical Therapy

NSAIDs and/or Corticosteroids

DMARDs (disease modifying anti-rheumatoid drugs)


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Surgery

As noted above, this type of arthritis is of autoimmune etiology. There ISsignificant swelling of the affected joints. Systemic symptomatology is also seenvery commonly. This includes fever, rash, night sweats, LAD and others. The

blood work will show evidence of marked generalized inflammation such as anelevated ESR (erythrocyte sedimentation rate)...also known as a sed rate.Patients frequently also have a positive test for Rheumatoid Factor (RF) in there

blood, although not all patients with RA have RF. This disease freqeuntly leadsto long term bone and joint deformities and disability. Here is an image showingswelling of the synovial membrane:

These images show common upper extremity deformities on x-ray and externally

(ignore the fact that rheumatoid is spelled wrong on the lower image!):


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Treatment of RA involves the use of anti-inflammatory agents (steroids andNSAIDs), immune suppresants and agents that are classified as DMARDs(disease modifying anti-rheumatoid drugs). This last category will help slow

down the progression of the disease, but most of the agents are expensive,injectable and associated with adverse effects.

This is brief summary of a few of the DMARDs:

Traditional DMARDs can be grouped in different categories and include:

Anti-malaria medications, particularly Plaquenil

Arava

Organ antirejection drugs, such as cyclosporine

Miscellaneous drugs, such as Azulfidine and gold

Chemotherapy drugs, such as methotrexate, Imuran, and Cytoxan

Here is a little specific information on some agents specifically:

Gold

Gold has been used as a medical treatment for centuries and was a

mainstay of RA treatment from the 1920s to the mid 1980s. Currently it is a

rarely used treatment for RA as newer medications are more effective.


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Gold works by decreasing inflammation in the joints, although doctors don't

know how it does this. Gold is given orally or by injection into the muscle.

The injection is more effective than the oral version.

Possible side effects include skin rash, anemia, low white blood cell count,

or liver and kidney problems.

Methotrexate

The most commonly used DMARD is methotrexate. Since the early 1980s,

methotrexate has gained prominence as an effective treatment for RA. It

also has advantages in having dose flexibility, as higher doses may be

used for worse disease, and it is easy to monitor for side effects by testing

for liver function and blood counts.

Side effects of methotrexate include rash, mouth sores, hair loss, fatigue,

liver inflammation, and bone marrow toxicity. The risk of side effects can

be reduced by taking daily folic acid.

Imuran

Imuran (azathioprine) is a chemotherapy drug that can be effective for RA,

particularly for complications such as vasculitis. It is an oral tablet. Side

effects include nausea, vomiting, rash, mouth sores, liver and blood count

abnormalities, and increased risk of infection. Regular blood test

monitoring is mandatory.

Anti-malaria Drugs (Plaquenil)

Plaquenil (hydroxychloroquine) is a drug used to treat malaria. It was

discovered that it worked for arthritis when people taking the drug for

malaria reported improvements in their arthritis. The drug affects the

immune system, although doctors do not know precisely how it works to

improve rheumatoid conditions.

Usually Plaquenil is used when other RA treatments fail. It can be given

along with steroid treatment to reduce the amount of steroid needed. It is

also given to treat the facial rash oflupus.

Plaquenil is given by mouth daily. Side effects include low white blood cell

counts, blood or protein in the urine, nausea, and skin rashes. High doses

can rarely cause injury to the back of the eye (retina); therefore, patients

on this drug should see an eye doctor every six to 12 months.


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The newest class of drugs used in the treatment of RA are theBiological

Response Modifiers. Most of these agents interfere with the action of

inflammatory mediators like Tumor Necrosis Factor (TNF) and others:

Biologic response modifiers Biologic response modifiers,

also known as biologics, are medications that were designed to

prevent or reduce the inflammation that damages joints.

Biologics target molecules on cells of the immune system, joint,

and the products that are secreted in the joint, all of which can

cause inflammation and joint destruction. There are several types

of biologics, each of which targets a specific type of molecule

involved in this process (tumor necrosis factor, interleukin-1, and

cell surface molecules on T and B lymphocytes). (See "Overview

of biologic agents in the rheumatic diseases").

Biologics that bind tumor necrosis factor (TNF), called anti-

TNF treatments, include Etanercept (Enbrel), adalimumab

(Humira), and infliximab (Remicade). These are called

anti-TNF agents.

Anakinra (Kineret) inhibits interleukin-1. Anakinra is

significantly less potent than TNF inhibitors in most people

with rheumatoid arthritis. It is occasionally recommended

for selected individuals who do not respond to anti-TNFagents. Anakinra cannot be used at the same time as anti-

TNF agents due to the risk of infection.

Abatacept (Orencia) interferes with the activation of T

cells. Abatacept is usually recommended only for people

with moderate or severe rheumatoid arthritis that is not

controlled with methotrexate and an anti-TNF agent. (See

"T cell targeted therapies for rheumatoid arthritis").

Rituximab (Rituxan) depletes B cells. Rituximab is usuallyrecommended only for people with moderate or severe

rheumatoid arthritis that is not controlled with

methotrexate and an anti-TNF agent. (See "Rituximab and

other B cell targeted therapies for rheumatoid arthritis").


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Summary of primary points:

1. RA is a systemic autoimmune disease that is characterized by immuneand inflammatory destruction of the synovial tissue.2. It often lead to significant deformity and disability

3. Systemic symptoms are frequently present4. Treatment involves the use of steroids, NSAIDs, DMARDs and Biologicresponse modifiers.

Ankylosing SpondylitisThis disease is not very common, but when you see a patient with it...you will notforget them. This disease eventually causes complete calcification of theintervertebral discs, leading to an inability to bend over at all. The spinedeformity as seen radiographically is termed, bamboo spine.

Chronic, inflammatory disease involving fusion of the joints of thespine and sacroilium

Genetic basis (HLA-B27)More prevalent in men

Here is a radiographic image of the lower spine:

Note how the intravertebral discs are as dense as the vertebrae themselves.So, in summary, Ankylosing spondylitis is a genetic disease seen usually inyoung males. The genetic marker that is tested for is called HLA - B27. This test

is specific for this disease. Finally, calcification of the inter-vertebral discs is theprimary symptomatic pathology.


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GOUT

Arthritis caused by precipitation of uric acid in the joint structuresUric acid deposits called Tophi

Seen more frequently in malesUric acid comes from metabolism of purines

Trauma is aggravating factor

Clinical Manifestations:

HyperuricemiaGouty arthritis

Tophaceous gout (crystal deposition)

Renal CalculiMost common joint involved is the metatarsophalangeal joint of

the great toe

Treatment:NSAIDsAllopurinol (lowers uric acid levels)ColchicineCorticosteroidsNarcotics

Patients with gout usually have elevated serum uric acid, but not always. This isan image of acute gout in the MTP joint of the great toe:

Pretty....isnt it?!You can see why this is very painful. The diagnosis is usually made on historyand physical alone. Rarely, aspiration of the affected joint is required. If this


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aspirate contains uric acid crystals, they will look like this under a polarizingmicroscope:

The treatment of gout involves both acute and prophylactic treatment.

Prophylactically, in patients with chronically elevated serum uric acid levels, we

will use a drug called allopurinol (Zyloprim ). This drug is taken orally,

usually two to three times per day. This drug acts by inhibiting enzymes in

the uric acid production pathway...thus leading to decreased serum uric

acid.

The acute treatment of gouty attacks involves NSAIDs (frequently a very

old one called Indomethacin (Indocin). This agent is often combined

with another drug that has been around for quite a while called Colchicine.The dosing of this agent is unusual. Usually we have the patients take two

tablets followed by one every hour until diarrhea starts. They then stop

and repeat the process in about twelve hours. Rarely, colchicine can

cause Aplastic Anemia, which is complete bone marrow suppresion. If

the patient notices bruising or bleeding...they need to be seen and tested

immediately.

Fibromyalgia

FibromyalgiaCharacterized by diffuse musculoskeletal pain, fatigue and trigger

points

Much more common in womenEtiology unknown

Diagnosis made when all other differential diagnoses are rules out

(see Table 41-8, pg. 1401)


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Treatment:

NSAIDsRest / exercise

Tricyclics

Fibromyalgia is a very controversial diagnosis. As noted, there is nospecific test for this disorder. The diagnosis is usually made when allother disorders have been ruled out. This disorder is most likely a

combination of different disorders with the commonality of trigger pointmuscle pain and fatigue. In some patients, there may be associatedpsychiatric issues like depression...although this can not be said for allpatients with fibromyalgia. For those interested, this is an excellent, up todate summary of this disorder:

http://www.mayoclinic.com/health/fibromyalgia/DS00079

Finally, I want to discuss hormone replacement therapy (HRT) in post-menopausal women and the controversial issues surrounding it.

First of all...lets look at estrogen and its role in female physiology:

Estrogen contributes to the development of secondary sex characteristics,which are the defining differences between men and women that dontrelate to the reproductive system. In women, these characteristics includebreasts, a widened pelvis, and increased amounts of body fat in the

buttock, thigh and hip region. Estrogen also contributes to the fact thatwomen have less facial hair and smoother skin then men.

Estrogen is an essential part of a womans reproductive process. Itregulates the menstrual cycle and prepares the uterus for pregnancy byenriching and thickening the endometrium. Two hormones, the luteinizinghormone (LH) and the follicle stimulating hormone (FSH), help to controlhow the body produces estrogen in women who ovulate.

Estrogen is manufactured mostly in the ovaries, by developing eggfollicles. In addition, estrogen is produced by the corpus luteum in theovary, as well as by the placenta. The liver, breasts and adrenal glandsmay also contribute to estrogen production, although in smaller quantities.

Estrogen can be broken down into three distinct compounds: estrone,estradiol and estriol. During a womans reproductive life, which starts withthe onset of menstruation and continues until menopause, the main type ofestrogen produced is estradiol. Enzymatic actions produce estradiol from


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androgens. Testosterone contributes to the production of estradiol, whilethe estrogen estrone is made from andostenedione.

Now...progesterone:

Progesterone is sometimes called the "hormone of pregnancy",[25] and ithas many roles relating to the development of the fetus:

Progesterone converts the endometrium to its secretory stage

to prepare the uterus for implantation. At the same time

progesterone affects the vaginal epithelium and cervical mucus,

making the mucus thick and impermeable to sperm. If pregnancy

does not occur, progesterone levels will decrease, leading, in the

human, to menstruation. Normal menstrual bleeding is progesterone

withdrawal bleeding.

During implantation and gestation, progesterone appears to

decrease the maternal immune response to allow for the acceptance

of the pregnancy.

Progesterone decreases contractility of the uterine smooth

muscle.[25]

In addition progesterone inhibits lactation during pregnancy. The fall

in progesterone levels following delivery is one of the triggers for

milk production.

A drop in progesterone levels is possibly one step that facilitates the

onset of labor.

The fetusmetabolizes placental progesterone in the production of adrenal

steroids.

This explains why progesterone only oral contarceptive pills (OCPs) work.

They basically fool the body into believing that it is pregnant.

The use of postmenopausal hormone replacement therapy (HRT) has

changed markedly over the last ten years. About eight years ago, two

major studies were done that showed that HRT is associated with a marked

INCREASE in the frequency of strokes and cardiac events. Prior to that, it


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was believed that HRT protected women from cardiovascular disease and

stroke. Now, the decision to place a woman on HRT depends on

developing an individualized risk/benefit profile for that patient. The

potential benefits of HRT are relief of vasomotor symptoms (hot flashes),

mood fluctuations and vaginal atrophy and/or dryness. Also, there is some

protection given against the worsening of osteoporosis. So, in summary,

one must weigh these potential benefits against the potential risks in light

of the degree of the patients symptoms and how much they interfere with

her life, the family risk of MI and CVA, smoking history and osteoporosis

prevalence in the family.

RENAL / UROLOGIC PATHOPHYSIOLOGY and PHARMACOLOGY

Kidney Stones

Kidney Stones (also called urolithiasis and nephrolithiasis) relatively

common problem seen more frequently in men than women. Stones can

be formed out of many different substances, however in order of

frequencythese are the most common:

Calcium Oxalate (and other salts of calcium) - > 75%

Struvite bacterial products that harden

Uric acid usually in patients with high serum levels ofuric acid like patients with Gout.

When a stone acutely obstructs the flow of urine (in the ureter), this

causes intense pain. Difficulty urinating may also occur. Acute

symptoms include lower abdominal pain (frequently radiating to the

groin and back), hematuria and diaphoresis. A patient who develops

kidney stones will often have reoccurrences. The most common

methods of making the diagnosis are helical CT scan and/or an

intravenous pyelogram (IVP). In the IVP, the patient is injected with

x-ray contrast material (usually iodinated) and xray images areobtained at several intervals after the contrast is administered.

Images are obtained from several different angles as well.

Obstruction of a ureter usually appears as Hydroureter ( a large

dilated ureter) and/or hydronephrosis (a large dilated kidney).


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Once the diagnosis is made, treatment depends upon the size and

location of the stone. Most stones less then 5mm will be passed

without need for intervention. Depending on many factors, the

patient can be treated in the hospital or at home. They are

instructed to drink lots of water, take pain medicine as prescribed and

strain the urine. This is done in order to chemically evaluate the

stone and then provide preventive therapy depending on the

underlying issues.

If the stone is not passed or the pain is severethe urologist will

surgically retrieve the stone. A stent is then placed in the ureter to

prevent further obstruction due to spasm. This is removed after 4 to

6 weeks.

Chronic obstruction of urine flow will lead to chronic kidney infection

and eventual renal failure.

Vasovagal syncope (or idiopathic orthostatic hypotension) this is a

condition that occurs infrequentlybut usually affects females less then 30

years of age. They have dizziness and light headedness that arises when

they stand up. This may lead to frank syncope. This condition is usuallydiagnosed after a long work-up looking for more common disorders. The test

used to make this diagnosis is called the Tilt Table Test. This changes the

patients body position and they are assessed for the development of

symptoms as described and changes in vital signs. Once diagnosed, patients

are often treated with a medication called:


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Fludrocortisone (Florinef) - Mineralocorticoids act on the distal tubules of thekidney to enhance the reabsorption of sodium ions from the tubular fluid into the plasma;

they increase the urinary excretion of both potassium and hydrogen ions. Theconsequence of these three primary effects together with similar actions on cation

transport in other tissues appear to account for the entire spectrum of physiologicalactivities that are characteristic of mineralocorticoids. In small oral doses, fludrocortisone

acetate produces marked sodium retention and increased urinary potassium excretion. Italso causes a rise inblood pressure, apparently because of these effects on electrolyte

levels. In summary, this medication increases the intravascular volume by increasingNA+ and H20 retention (like aldosterone), and this improves cerebral perfusion when

standing.

Know the major indications and adverse effects for the antibiotic

metronidazole (FLAGYL) Interferon alphais an agent that occurs naturally as a cytokine

(interleukin). We use it to treat chronic viral hepatitis. It often

produces severe and debilitating flu-like adverse effects.

Know the indications, mechanism of action and adverse effects

associated with the statin drugs like lovastatin (Mevacor)

Know the indications, mechanism of action and adverse effects

associated with nitroglycerine.

Understand the major differences in bacterial coverage between the

first generation and later generation cephalosporins

Repeating the information listed on the previously distributed Final

Exam Study Guide, make sure that you review the cardiovascular

material including:

o inotropes and chronotropes (what they are and some examples

of eac h)

o Goals of treatment for CHF

o Basic issues regarding the use of Digitalis

o Ace inhibitors and ARBs

o Basic issues concerning the diuretics (HCTZ, K+ - sparing and

loop diuretics)o Use ofwarfarin (Coumadin ) and Heparin (non-fractionated and

lovenox)o Differential diagnosis of chest pain

o Angina and MI presentation, diagnosis (including serum tests

and EKG findings) and basic treatment

Side effects oftetracycline


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Pulmonary physiology, disorders, diagnosis and treatment

o COPD

o PFTs

o Asthma (including prophylactic and acute treatment)

o

- 1 antitrypsin deficiencyo Pulmonary embolus

Basic facts regarding Anemia:

defined as a condition that results in impaired oxygen

carrying capacity and delivery of blood.

General symptoms include fatigue, SOB, pale skin

There are many different types and etiologies

For our purposes, they are grouped into two sets of two:

MACROCYTIC / HYPERCHROMIC large, very red erythrocytes andMICROCYTIC / HYPOCHROMIC small, pale erythrocytes. In the basic CBCtest, you will find the MCV (mean corpuscular volume) and the MCHC (mean

corpuscular hemoglobin concentration). The MCV gives us information

regarding the SIZE of the RBC. The MCHC gives us information regarding

the color (or richness of hemoglobin) of the RBC. So, in a patient with a

macrocytic/hyperchromic anemia, the MCV and MCHC will be elevated. In a

patient with a microcytic/hypochromic anemia, the MCV and MCHC will both

be low.

The macrocytic/hyperchromic examples we should remember are B12

deficiency anemia (also called pernicious anemia) and Folate deficiency

anemia. I realize that some of your references may have categorized the

size and/or color of the RBC as somewhat differentbut after these

disorders are present for some time in a patient, these size and color

features will be present. The microcytic/hypochromic examples include iron

deficiency anemia and anemia of chronic disease.

B12 deficiency anemia used to be very common before we understood theissues and sources of B12. During the last decade, cases of B12 deficiency

are increasing due to the frequency of surgery for Crohns disease (where

they might remove the ileum this is where B12 is absorbed) and gastric

bypass surgery. Bariatric surgery can lead to B12 deficiency secondary to

loss of a protein produced in the stomach called intrinsic factor (IF) which is


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very helpful in terms of the absorption of B12. Since the stomach is

bypassed in this surgery, IF can not be released into the gut and accompany

vitamin B12 to the ileum where it absorbed. Patients who have had bariatric

surgery will need to take large amounts of B12 orally for the rest of their

lives to make sure that deficiency does not occur. Even though they do nothave the benefit of IF, they can absorb enough B12 orally to prevent

deficiency. Patients who have had their ileum removed due to Crohns

disease (or anything else) NEED to have monthly B12 IM injections. B12

deficiency anemia produces the general symptoms of anemia as delineated

above, however, if present for more the 7 or 8 years, B12 deficiency leads

to irreversible neuropsychiatric issues similar to Alzheimers Disease and

schizophrenia. It has been suggested that more then 25% of patients who

were kept in insane asylums in the 1800s had B12 def. psychosis.

Folate deficiency is best known for the fact that if women are pregnant and

folate deficient during the first trimester, there is a much higher risk for

the development of neural tube birth defects like spina bifida. For this

reason, it is recommended that ALL women of child bearing age take a daily

multivitamin with folate as they may become pregnant and be unaware that

they are for several weeks after conception.

Iron deficiency is relatively rare in developed society as iron is found in

protein rich foods. This includes cheap foods like Mcdonalds,etcThe most

common etiology of iron deficiency in developed countries is NOT DIETARY

DEFICIENCY but menorrhagia (or heavy periods). Even women whose

menstrual period flow is on the upper side of normal can become significantly

iron deficient. Also, occult GI bleeding like colon cancer and polyps can end

up iron deficient. Treatment includes fixing the underlying problem (like

giving hormone pills to women to regulate their periods). and then providing

supplemental iron.

Anemia of chronic disease is extremely common and occurs in those with

any chronic disease including COPD/Cancer/ Heart disease, etcMostnursing home residents probably have this to some degree. The degree of

anemia seen with this disorder is not as dramatic as with the other anemias.

For all intensive purposes, it looks a lot like iron deficiency anemia.but the

patients iron stores (reflected in serum Ferritin concentration) are

NORMAL. They have iron.they just can not utilize it. This condition is


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usually not treated unless their hemoglobin level drops enough to cause

symptoms.

A Few Renal Issues:

Renal hormonesVitamin D activated through reaction in kidneys Erythropoietin stimulates bone marrow to produce RBC in

response to hypoxiaReleased from kidneys in response to renal tissue hypoxiaLack of it Anemia of chronic renal failure


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path/pharm summaries ms/gi/heme/renal

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