study guide for mss, cns

8/18/2019 Study Guide for MSS, CNS

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1. What are the organic and inorganic components of the bone?

a. Organic the cells in the bone and the protein (mainly type I collagen)

i. Osteoprogenitor cells

ii. Osteoblasts

iii. Osteocytes

iv. Osteoclasts

b. Inorganic: calcium hydroxyapatite responsible for the hardness of the bone

2. What are the causes of developmental anomalies of the bone?

Give examples of these developmental anomalies.

a. Genetic alteration in the that affect transcription factors, especially those coded byHOMEOBOX GENES

Examples:

Failure of dev’t

Formation of extra

bones Syndactylism

Arachnodactylism

3. Give the basic defect and describe the pathologic finding in the following:

a) Achondroplasia

Basic defect: disorganized chondrocytes

Pathologic findings: premature deposition of bone and sealing of growth plateb) Osteogenic imperfecta

Basic defect: too little bone

Pathologic finding: fractures, blue sclerae, hearing loss, dental imperfectionsc) Osteoporosis

Basic defect: increased porosity reduced bone mass

Pathologic findings: asymptomatic until well-advanced, fractures and deformities, loss of

height.d) Avascular necrosis

Basic defect: bone necrosis caused by ischemia

Pathologic findings: subchondral pain, bony collapse, medullary paine) Brown tumor

Basic defect: microfractures and secondary hemorrhages

Pathologic findings: irregular bone resorption, microfracture, macrophage and connectivetissue proliferation.

4. What is renal osteodystrophy? What are the skeletal changes seen?

It is used to describe collectively all of the skeletal changes of chronic renal disease, including(1) increased osteoclastic bone resorption mimicking osteitis fibrosa cystica, (2) delayed matrixmineralization (osteomalacia), (3) osteosclerosis, (4) growth retardation, and (5) osteoporosis. Asadvances in medical technology have prolonged the lives of individuals with renal disease, its impact onskeletal homeostasis has assumed greater clinical importance.

The various histologic bone changes in individuals with end-stage renal failure can be dividedinto three major types of disorders. High-turnover osteodystrophy is characterized by increased boneresorption and bone formation, with the former predominating. In contrast, low-turnover or aplastic disease is manifested by adynamic bone (little osteoclastic and osteoblastic activity) and, less



commonly, osteomalacia. Many affected individuals have the third type, which is a mixed pattern of disease.

Robbins p.2284

5. Briefly describe the process (or sequence) in the following?

a. Fracture healing p. 2286

1. Organization of hematoma- fibrin mesh (seals off fracture site)- growth factor activate cells- procallus

2. Conversion of procallus to fibrocollagenous callus- stabilizes fracture site- undergoes endochondral ossification

3. Maturation of bony callus

What are the factors that may hinder fracture healing?Fragments of splintered boneInadequate mobilizationInfectionInadequate minerals/Vitamin DUnderlying disease

b. Pyogenic osteomyelitis p. 2289

Pyogenic osteomyelitis is almost always caused by bacteria. Organisms may reach the bone by(1) hematogenous spread, (2) extension from a contiguous site, and (3) direct implantation. Inotherwise healthy children, most cases of osteomyelitis are hematogenous in origin and develop in the

long bones. The initiating bacteremia may stem from seemingly trivial injuries to the mucosa, such asmay occur during defecation or vigorous chewing of hard foods, or minor infections of the skin. In adults,however, osteomyelitis more often occurs as a complication of open fractures, surgical procedures, anddiabetic infections of the feet.

6. Briefly discuss the pathogenesis, incidence, clinical and morphologicfeature of the ff:

PATHOGENESIS INCIDENCE CLINICAL MORPHOLOGICRHEUMATOIDARTHRITIS

triggered by exposureof a genetically susceptible host to anarthritogenic antigenresulting in abreakdown of immunological self-tolerance and achronic inflammatoryreaction.

continuing autoimmunereaction, the activationof CD4+ helper T cells,and the local release of inflammatorymediators andcytokines thatultimately destroys the joint

About 1% of world'spopulation

Women three to fivetimes more thanmen.

Most common in 40to 70 years old, butno age is immune.

begins slowly andinsidiously

Initially there ismalaise, fatigue, andgeneralizedmusculoskeletal pain,and only after severalweeks to months dothe joints becomeinvolved.

Symptoms usuallydevelop in the hands(metacarpophalangeal and proximalinterphalangeal joints)and feet, followed bythe wrists, ankles,elbows, and knees.

(1) infiltration of synovial stroma(mostly CD4+ helper T cells)(2) increasedvascularity due tovasodilation andangiogenesis(3) aggregation of organizing fibrin(4) accumulation of

neutrophils in thesynovial fluid andalong the surface of synovium(5) osteoclasticactivity(6) pannusformation.



OSTEOARTHRITIS

multifactorial diseasethat has genetic andenvironmentalcomponents.

genes involved inprostaglandinmetabolism and WNTsignaling. The major environmental factorsrelate to aging andbiomechanical stress,which is influenced byobesity, musclestrength, and jointstability, structure, andalignment.

age of 50

80% to 90% haveevidence of thedisease by age 65.

Characteristicsymptoms includedeep, achy pain thatworsens with use,morning stiffness,crepitus, andlimitation of range of movement.

Heberden nodes,prominentosteophytesat the distalinterphalangeal joints,are common inwomen (but not men).

early stages -chondrocytesproliferate, formingclusters.

Mushroom-shapedosteophytes (bonyoutgrowths)develop at themargins of thearticular surface andare capped byfibrocartilage andhyaline cartilagethat gradually ossify.

GOUT Uric acid is the endproduct of purinemetabolism. Approximately 90% of

the filtered urate isreabsorbed, and theurate transporter 1gene (URAT1) has animportant role in thereabsorption process.Decreased filtrationand underexcretion of uric acid underliesmost cases of primarygout.

More than 10% of thepopulation of theWestern

hemisphere

prevalence isincreasing;

develops in fewer than 0.5% of individuals

(1) asymptomatichyperuricemia(2) acute goutyarthritis, (3)

intercritical gout, and(4) chronictophaceous gout.

(1) acute arthritis(2) chronictophaceous arthritis(3) tophi in various

sites (4) goutynephropathy

INFECTIOUSARTHRITIS

Articular structurescan also becomeinfected by directinoculation or fromcontiguous spreadfrom a soft-tissueabscess or focus of osteomyelitis.

People with artificial joints are more atrisk than gen.population but haveslightly differentsymptoms, areinfected withdifferent organismsand require differenttreatment.

potentially seriousbec. it can causerapid destruction of the joint and producepermanentdeformities.

Microorganisms of all types can seed joints duringhematogenousdissemination.

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7. What immunostains are used in identifying sarcomas?

TFE3 protein, CD30, CD35, CD56, EMA, Ewing sarcoma (013), Friend LeukemiaIntegration 1, Herpes Virus 8, HMB45

8. Give the bases for grading and staging the tumors

a) Grading of Bone tumors-cellularity and nuclear features of the tumor cells are important criteria used for grading:

-irregularity of the nuclear contours, enlargement and hyperchromasia of the nuclei arecorrelated with grade- Mitotic figures and necrosis are also useful in grading

Low grade (Broder’s classification): Grade 1 and 2High grade (>25% chance of metastasis): Grade 3 and 4

b) Staging of Bone tumors-done with: (1) the assessment of the surgical grade (G), (2) the local extent (T) and (3)the

presence or absence of regional or distant metastasis- The anatomic extent (T) is subdivided according to whether the lesion is intracompartmental

(A) or extracompartmental

- Presence or absence of metastasis (M) is the 3rd

major factor related to both prognosis andsurgical planning

9. Define/describe the following:

a. Pott’s disease

-also known as tuberculous spondylitis-Pathogenesis: usually secondary to an extraspinal source of infection. Pott disease

manifests as a combination of osteomyelitis and arthritis that usually involves more than 1vertebra. The anterior aspect of the vertebral body adjacent to the subchondral plate is usuallyaffected. Tuberculosis may spread from that area to adjacent intervertebral disks. In adults,

disk disease is secondary to the spread of infection from the vertebral body. In children, thedisk, because it is vascularized, can be the primary site.

Progressive bone destruction leads to vertebral collapse and kyphosis. The spinal canalcan be narrowed by abscesses, granulation tissue, or direct dural invasion, leading to spinalcord compression and neurologic deficits.

The kyphotic deformity is caused by collapse in the anterior spine. Lesions in thethoracic spine are more likely to lead to kyphosis than those in the lumbar spine. A coldabscess can occur if the infection extends to adjacent ligaments and soft tissues. Abscesses inthe lumbar region may descend down the sheath of the psoas to the femoral trigone region andeventually erode into the skin.

Conditions to consider in the differential diagnosis of Pott disease include the following:

Spinal tumors Mycobacterium kansasii Nocardiosis Paracoccidioidomycosis Septic arthritis Spinal cord abscess Tuberculosis

b. Scrofula

a. Scrofula is the Latin word for brood sow, and it is the term applied to tuberculosis of the neck. Cervical tuberculosis is usually a result of an infection in the lymph nodes,

known as lymphadenitis. Extrapulmonary tuberculosis, such as scrofula, is observed

most often in individuals who are immunocompromised, accounting for up to 50% of

these cervical infections.

Pathogenesis: Mycobacterium tuberculosis is an obligate aerobe, non–spore-forming, slender rod. Humans are its only reservoir. Transmission is from person toperson via respiratory route by inhalation of small aerosols. After a short period of replication in the lungs, silent dissemination occurs through the lymphohematogenoussystem to extrapulmonary sites, including the cervical lymph nodes.

A study by Bruzgielewicz et al of patients with head and neck tuberculosis found



that among the 26 patients with lymph node tuberculosis, 15 patients had infectedlymph nodes of the second and third cervical regions and 11 had infected lymph nodesof the first cervical region.[1]

Nontuberculous mycobacterium (NTM) differs from M tuberculosis in 2 respects:person-to-person transmission generally does not occur, and NTM species areubiquitous in nature and not necessarily pathogenic or equated with disease. The oralcavity may serve as a common portal of entry because the disease primarily occurs inchildren who have a propensity to put contaminated objects in their mouth

c. Osteochondroma-a Chondrogenic Tumors (Cartilage-forming)-most frequent benign tumor in children

Site: Metaphysis, cortex of long bones (lower femur, tibia, humerus)Pathogenesis: Displacement of the lateral portion of the growth plate which thenproliferates diagonal to the long axis of the bone and away from a nearby jointMorphology: Mushroom-shaped with cartilage

d. Osteoid osteoma

- An Osteogenic tumor (Bone-forming)

- Round to ovoid mass with nidus affecting the cortex of the metaphysis

- Very painful due to prostaglandin metabolites

- Responds to analgesics

- Elicits tremendous amount of the reactive bone formation that encircles the lesion

e. Chondroma

- Chondrogenic tumor

- Benign tumor of hyaline cartilage

- Site:

Medullary cavity---endocohondroma (most common intraosseus cartilage tumor)

On the surface of bone-----subperiosteal/juxtacortical chondroma

Affects the short tubular bones of ahnds and feet

- Pathogenesis:

Deviations from rests of growth plate cartilage

Subsequent proliferation and enlargement

- Associated syndromes:

Ollier’s disease: multiple endohromas, unilateral distribution

Maffucci’s syndrome: Endochromatosis + soft tissue hemangiomas

-Morphology: Nodule of Benign hyaline cartilage- Clinical manifestations:

* Asymptomatic, occasionally painful and cause fractures, C or O ring sign on x-ray

f. Chondroblastoma

- Rare benign tumor

- 1% of primary bone tumors

- Site:

Epiphyses and apophyses

Most ommonly arise in the knee

Other sites: pelvis and ribs in older patients

- Morphology:

Polyhedral chondroblast

Mitosis and necrosis

Chicken-wire appearance

-Clinical manifestations: painful, located near the joints and on x-rays: Well-defined

geographic lucency

g. Osteoma

- Round sessile tumor made up of woven and lamellar bone affecting cortical surfaces of

flat bones

- May cause obstruction of sinuses and impingement of other structures

- Do not transform into osteosarcoma

h. Fibrous dysplasia

A localized developmental arrest

Normal bone components are present but did not mature

Clinical patterns:

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a. Monostonic: 70%; single bone involvementb. Polyostotic without endocrine dysfunction: 27%, early manifestationc. Polyostotic with café au lait and endocrinopathies: McCune Albright sundrome-

precocity, hyperthyroidism, pituitary adenoma, adrenal hyperplasia

Morphology:a. Gross: inmtramedullary, well-circumscribed, grittyb. Micro: curvilinear trabeculae of woven bone surrounded by fibroblasts (Chinese

letters); no osteoblastic rimming

i. Rheumatoid nodule

Most common cutaneous lesion

Arise in regions that are subjected to pressure

Firm, non-tender and round to oval

Arise in the subcutaneous tissue

j. Tophus (Tophi)

Aggregates of urates surrounded by an inflammatory reaction with lymphocytes,macrophages and foreign body giant cells (Pathognomonic hallmark of gout)

k. Heberden’s nodes

Bony enlargements in the fingers; usually found in women

l. Red neuron- is an ischemic cell changem. Cachexia- weakness and wasting of the body due to severe chronic illness

n. Contusion- is a type of TRAUMA, blunt trauma, coup and countercoup lesions

o. Incision- type of trauma, a penetrating injury, sharp object

p. Perforation- hole made by piercing, aperture passing through or into something

10. Define and briefly explain the pathogenesis

Parkinson’s disease

- It is a chronic and progressive movement disorder; it primarily affects the substantia nigracausing a decrease/ lack of dopamine.

- (+) paucity of movement

- Primary motor signs of Parkinson’s disease include the following: tremor, bradykinesia,

rigidity, & postural instability.

- Loss of cathecolaminergic neurons: Lewy Bodies

Pathogenesis: (+) reduction of striatal dopamine

Guillain – Barre Syndrome “Galing - Baba”

- It is rare but serious autoimmune disorder in which the immune system attacks healthy

nerve cells in the peripheral nervous system.

- It’s a progressive ascending paralysis

- S/sx: tingling or prickly sensations (most common), muscle weakness, difficulty walking

steadily, severe lower back pain, loss of bladder control, fast heart rate, difficulty

breathing & paralysis.

Pathogenesis: absence/ delayed conduction in action nerve fibers --> (+) aberrant conduction



--> demyelination of peripheral nerves = (+) Paralysis

Multiple Sclerosis- It is the most common type of demyelination disease, causing disruption of the myelin

that insulates and protects nerve cells.- It is also an Autoimmune Disease with a relapsing and remitting course.- Female > Male- S/sx: weakness, fatigue, paralysis, vertigo or dizziness, erectile dysfunction, incontinence,

muscle spasticity & etc.

Pathogenesis: (+) inflammation of myelin sheath --> T cells (-) recognize the cells that needsto destroy “ Autoimmune dis.” --> (+) distruction of myelin sheath = (+) loss of electrical conduction.

Progressibe multifocal leukocephalopathy- A neurological disorder characterized by or destruction/inflammation of the white matter of

the brain at multiple locations (multifocal).- Caused by a viral infection : JC virus

- S/sx: clumsiness, progressive weakness and visual, speech, and sometimes personalitychanges

Pathogenesis:

Huntington Disease- It is an Autosomal dominant disease, characterized by movement chorea, athetosis or

choreathetosis.- (+) atrophy of the caudate nucleus, putamen, globus pallidus, subthalamic nuclei.- S/sx: Involuntary jerking or writhing movements (chorea), Muscle problems (dystonia), Slow

or abnormal eye movements, Impaired gait, posture and balance, Difficulty with thephysical production of speech or swallowing.

Pathogenesis: (+) Loss of striatal inhibitory output to the globus pallidus --> inhibitory outputto the subthalamic nucleus --> (+) regulatory motor activity = (+) Choreoathetosis

Amyotrophic lateral sclerosis “Without nourishment“- This is a specific disorder that involves the death of neurons.- Affects both upper and lower motor neurons- Variants: Progressive Muscular Atrophy (predominance of lower motor neuron

dysfunction) & Progressive Bulbar Palsy (predominance of cranial nerve and brainsteminvolvement).

- S/sx: Maladaptive social behavior, Wrist drop interfering with work performance, Aspiration ,Slurred speech, hoarseness.

Pathogenesis:In contrast to the advances in understanding the pathophysiology of ALS, however, the

mechanisms that lead to disease onset (ie, pathogenesis) remain unknown. It is reasonable toassume that the abnormal gene or gene product plays a role in triggering disease onset infamilial ALS and may have a role in disease propagation, but having an abnormal gene isneither necessary nor sufficient for developing ALS. Rarely, obligate familial gene carriers donot develop the disease. There is incomplete penetrance, or age-dependent penetrance, of theautosomal dominant genes.

Additional factors must be postulated to intervene between birth and disease onset



even in patients who develop familial ALS, because the disease does not appear to start atbirth, and within a given family there is great variability in the age of onset. Having normalcopies of these genes does not prevent development of sporadic ALS.

11. What are the reactions of the following cells to injury?

Neurons

Astrocytes

Microglia

Oligodendrocytes

Ependymal cells



12. Give the causes of:

a. Subarachnoid hemorrhage-Non-traumatic type of intracranial hemorrhage due to ruptured berry (saccular)aneurysm

b. Vasogenic edema-Extracellular edema caused by tumors, abscess, hemorrhage, and infarction

-Mechanism: increased vascular permeability

c. Hydrocephalus(a) Communicating: cerebrospinal fluid (CSF) is able to pass the subarachnoid

space (example: post meningitis)(b) Non-communicating / Obstructive: blockage in the CSF pathway within the brain

(example: stenosis of the cerebral aqueduct / tumor within the ventricle)

13. Differentiate the following as to site and causes:

14. Give the WHO grade of the following:

d. Pilocytic astrocytoma - I/IV (well differentiated or low grade)e. Glioblastoma - IV/IV (undifferentiated or high grade)f. Ependymoma - II/IV ( moderately differentiated or intermediate)g. Medulloblastoma - IV/IV (undifferentiated or high grade)h. psammomatous meningioma - I/IV (well differentiated or low grade)

Site Causes

Epidural hemorrhage

>95% are supratentorial

o temporoparietal:60%

o frontal: 20%

o parieto-occipital:20%

<5% are located infratentoriallyin posterior fossa

nerally unilateral

Tear of the middle meningeal artery

Children and Adults: usually with skullfracture

ants: may develop even without fracture(traumatic displacement of deformable

skull)

Subdural hemorrhage

Most common over the lateralaspects of cerebral hemispheres

and may be bilateral

lunt trauma without skull fracture, withtear of bridging veins

Adults: more common cases in elderlypatients due to brain atrophy wherein

bridging veins are stretched out,Infants: bridging veins are thin-walled,

becoming more fragile

Subarachnoid hemorrhage Intracranial(Subarachnoid space)

Ruptured berry (saccular) aneurysm

Intracerebral hemorrhage Intracranial(50-70% occurs in basal ganglia)

Hypertension



15. Briefly discuss the pathogenesis of the following

A. RABIES1) introduced through a bite, 2) the virus moves slowly as it jumps from nerve cell to

nerve cell 3) The time it takes the virus to go from the bite wound to the brain is theIncubation Period. 4) As soon as the virus reaches the brain it works its way into thesalivary glands where it replicates in abundance and is shed in the saliva. At this point theanimal becomes infectious and can transmit the disease through a bite. 5) the virus in thebrain has infected enough of the brain tissue that it begins to affect the animal's behavior

B. POLIOMYELITIS An Enterovirus Transmission is fecal-oral It infects tissues in the oropharynx, andsecreted into the saliva, then swallowed and multiplies in intestinal mucosa and lymphnodes. Manifests as transient viremia and fever. There is invasion of the CNS andreplication in motor neurons of the spinal cord (spinal poliomyelitis) or brain stem (bulbar poliomyelitis)

C. HERPEX SIMPLEX ENCEPHALITISHerpes simplex encephalitis (HSE) is an acute or subacute illness that causes both

general and focal signs of cerebral dysfunction. Brain infection is thought to occur bymeans of direct neuronal transmission of the virus from a peripheral site to the brain via thetrigeminal or olfactory nerve. The exact pathogenesis is unclear, and factors that precipitate

HSE are unknown

D. SUBACUTE SCLEROSING PANENCEPHALITISMeasles is an acute febrile exanthematous condition that is usually a self-limiting

disease, but it can be associated with a complication, subacute sclerosing panencephalitis(SSPE). It is a rare delayed complication of measles due to persistence of the virus in thecentral nervous system. All of the genetic analyses of viral material derived from braintissue of SSPE patients have revealed sequences of wild-type measles virus (MV). There isno evidence that measles vaccine can cause SSPE. Several mutations have beendescribed in genes coding for proteins in SSPE strains of MV. Several host cellmodifications, mechanisms of virus reactivation and immunopathology in pathogenesis of SSPE have been explained recently, broadening the understanding of this fatal disease.

E. CYTOMEGALO-INCLUSION DISEASE CID Almost always occurs in women who have primary CMV infection during pregnancy,

although rare cases are described in women with preexisting immunity who presumablyhave reactivation of infection during pregnancy. CID is characterized by intrauterine growthrestriction, hepatosplenomegaly, hematological abnormalities (particularlythrombocytopenia), and various cutaneous manifestations, including petechiae and purpura(ie, blueberry muffin baby). However, the most significant manifestations of CID involve theCNS. Microcephaly, ventriculomegaly, cerebral atrophy, chorioretinitis, and sensorineuralhearing loss are the most common neurological consequences of CID. Intracerebralcalcifications typically demonstrate a periventricular distribution and are commonlyencountered using CT scanning (see the image below). The finding of intracranialcalcifications is predictive of cognitive and audiologic deficits in later life and predicts a poor neurodevelopmental prognosis.

16. What are neural tube defects?

o Neural tube defects are the most common among the malformation & developmentaldiseases. This includes the following:

a. Anencephaly- most likely due to folate deficiencyb. Encephalocoele and meningoencephalocoele

c.Spina bifida, meningocoele and meningoencephalocoele (from defect of the caudalportion of the neural tube)

17. Describe the normal appearance of pleural fluid. Transudate: clear and pale yellow

18. In semen analysis, how do you determine the viability of thespermatozoa?

Viability is obsereved using supravital staining of a fresh sample with eosin stain. Viablesperm do not take up the stain; whereas dead sperm have damaged membranes andabsorb the stain. 100 sperm are counted and evaluated; percentage of dead sperm should



not exceed the percentage of immobile sperm. Normally, 50% or more of the sperm shouldbe viable.

19. In CSF examination, how will you differentiate a traumatic tap from apathologic bleed?

CRITERIA FOR IDENTIFYING A TRAUMATIC TAP 1. The number of RBC's diminishes greatly between the first and last tubes.2. The supernatant is not xanthochromic.3. The CSF white blood cell count is not higher than expected. (When blood has been in

the CSF for hours or days, it acts as an irritant and excites a CSF pleocytosis. In atraumatic tap, there should be 1 or 2 WBC's for every 1,000 RBCs if the patient's peripheral

blood counts are normal.)

20. Give the significance of the following findings in the CSF.a. Increased polymorphonuclear cells

o Bacterial and Fungal infectionsb. Increased lymphocytes

o Viral infectionc. Elevated protein values

o Normal: 15-45 mg/dl

o Increased in meningitis, hemorrhage and MSd. Decreased glucose levels

o Normal: 60-70% of plasma conc.o Decreased in bacterial, fungal, TB meningitis

e. Increased lactate

>35 mg/dl : bacterial

>25 mg/dl: TB and fungal meningitisf. Increased glutamine

Normal: 8-18 mg/dl

>35 mg/dl: assoc. with disturbances in consciousness

21. What is the mucin clot test? The string test? How do you interpretthe results?

o Mucin clot test Also known as the Rope’s test, is an estimation of the integrity of the hyaluronic acid-protein complex (mucin). Normal synovial fluid forms a tight ropy clot upon the addition of acetic acid. A good mucin clot indicates a good integrity of the hyaluronate. A poor mucinclot, one that breaks up easily, is associated with destruction of hyaluronate.

o String Test A string test can be used to evaluate the level of synovial fluid viscosity. Normal synovialfluid will form a “string” approximately 5cm long before breaking. In addition, the fluid maycling to the side of the test tube rather than running down to the bottom. Synovial fluids with

poor viscosity will form shoter strings (<3cm) or run out of the syringe and down the side of the test tube like water. Low viscosity of synovial indicates the presence of inflammatoryprocess

22. Describe the following synovial fluid crystal

Crystal Polarization microscopy Other identification

Monosodium urate Strong negative birefringence,needle-shaped, long

Uricase digestionX-ray diffraction

Calcium pyrophosphatedihydrate (CPPD)

Weak positive birefringence,rhomboid or small rods,pleomorphic

X-ray diffraction

Calcium Phosphate(hydroxyapatite

Not easily visualized Electron microscopyX-ray diffraction

Cholesterol Rhombic or plate-like, notchedcorners, multicolored, occasionallysmall and needle-like

Chemical determination



Corticosteroids Pleomorphic,variable birefringence

Follows intra-articular steroidtreatment

23. What are the effects of the following?

a) Ethanol – most widely used and abused agent throughout the world.

b) Cocaine – Psychomotor stimulant



c) Amphetamine – (Methamphetamine) Psychomotor stimulant

d.) Heroin – Opioid derived from the poppy plant

e. ) Acetaminophen – Forms a toxic metabolite which is detoxified by the gluthatione in the liver.

f. )Acetylsalicylic Acid – (Aspirin) Accidental ingestion of large number of tablets (usually children):ingestion of 2-4grams



d) Exogenous estrogen – (Hormone Replacement Therapy)

h.) Thalidomide

Before taking thalidomide, tell your doctor or pharmacist if you are allergic to it; or if you have any other allergies. This product may contain inactive ingredients, which cancause allergic reactions or other problems. Talk to your pharmacist for more details.

Before using this medication, tell your doctor or pharmacist your medical history,especially of: certain blood disorders (low platelet/white blood cell count),numbness/tingling of arms/legs, seizures.

Caution is advised when using this drug in people with HIV because they may bemore sensitive to the effects of the drug. While thalidomide is used to treat muscle wastingand other HIV-related conditions, the drug might affect the amount of HIV in your system(viral load). Therefore, the manufacturer recommends having HIV tests from time to time.

This drug may make you dizzy or drowsy. Do not drive, use machinery, or do anyactivity that requires alertness until you are sure you can perform such activities safely. Avoid alcoholic beverages.

Since this drug can be absorbed through the skin and lungs and may harm anunborn baby, women who are pregnant or who may become pregnant should not handlethis medication or breathe the dust from broken capsules.

Thalidomide must not be used during pregnancy due to the risk of severe birthdefects and other serious, sometimes fatal harm to an unborn baby. If you are female andbecome pregnant or think you may be pregnant, if your period is late or you have unusualmenstrual bleeding, or if you stop using 2 forms of birth control, stop taking thalidomide andtell your doctor right away. If you are male and have had unprotected sex with a womanwho can become pregnant, or if you think your sexual partner may be pregnant, tell both of your doctors right away. (See also Warning section.)

It is not known whether this drug passes into breast milk. Because of the possiblerisk to the infant, breast-feeding while using this drug is not recommended. Consult your doctor before breast-feeding.

24. Differentiate the following.

a. Heat cramps - loss of electrolytes via sweating, hallmark is cramping of voluntary musclesb. Heat stroke

- Thermoregulatory mechanisms fail, sweating ceases –-> rise in core body temp(>106ºF/40C)

- General peripheral vasodilatation (nitrosylation of RYR1 gene)- Rapid pulse & cardiac dilatation- Stimulation of respiratory centers :

Ryanodine receptor type 1 (RYR1): located in the sarcoplasmic reticulum; regulates the

release of calcium into the cytoplasm Cell necrosis either in the form of rhabdomyolysis or necrosis of the myocardium as a

consequence of RYR1 gene nitrosylation in skeletal muscle Mutations in RYR1 gene can also result in susceptibility to heat stroke and malignant

hyperthermia rise in temp and muscle contracture in response to certain anestheticsc. Heat exhaustion - most common heat syndrome due to failure of CVS to compensate for

Hypovolemia secondary to water depletion; Sudden prostration & collapsed. Malignant Hyperthermia - is a disease that causes a fast rise in body temperature and

severe muscle contractions when someone with the disease gets general anesthesia. It isinheritable.



25. Describe the effects of the following

a. Air blast - Violent increase in pressure in atmosphere; Epithelial shredding and tearing of tissue

b. Immersion blast - In water; hemorrhage & laceration of air-containing organc. Air Embolism

- May occur as complication of scuba diving, mechanical positive-pressure ventilator support, hyperbaric oxygen therapy

- Causes an abnormal increase in intra-alveolar gas pressure --> entrance of air into theinterstitium and small blood vessels Pulmonary, mediastinal or subcutaneous emphysema Coalescence of numerous small air emboli --> access to arterial circulation --> acute

stroke like symptoms/MI --> deathd. Decompression Sickness - Due to undissolved nitrogen gas bubbles in the circulation

Bends (periarticular) Chokes (lungs) CNS: visual disturbances, headache Caisson disease of bone: aseptic necrosis (femoral and humeral heads)

e. Acute Radiation InjuryFactors affecting radiation injury:

1. Type of radiation - Penetrability, energy & pattern of deposition2. Rate of delivery, Field Size - Lesser injury with fractional doses3. Radiosensitivity of cells - Rapidly-dividing cells are more sensitive4. Phase in cell cycle - Peak sensitivity at G2 phase & mitotic phase

5. Degree of oxygenation - Oxygen amplifies effect by formation of free radicals

Clinical Manifestations of Radiation Injury:1. Acute radiation syndrome / sickness Subclinical – mild nausea and vomiting (100% survival) Hematopoeitic – death w/in 3 wks pancytopenia --> bleeding, anemia, infection; May

require BM transplant GIT – death w/in 2 wks; Severe destruction of entire GIT epithelia --> diarrhea,

dehydration, septicemia CNS – death w/in 14-36 hrs; endothelial injury & neuronal injury --> cerebral edema,

convulsion, coma2. Radiation in medical treatment

- Compromised vascular supply- Replacement of normal parenchymal tissue by fibrosis scarring and loss of

function3. Growth & developmental abnormalities Pre-implantation pd – abortion Implantation-9th wk – congenital malformations Fetal period (9th wk-birth) – leukemia; other neoplasms Postnatal pd – abnormal bone growth & maturation

4. Chromosomal mutation5. Delayed radiation injury

Cancers due to radiation:

Basal & squamous cell Ca (skin)

Leukemia

Bone cancer (radium)

Lung cancer (uranum)

Thyroid cancer Most vulnerable sites of delayed radiation injury

BLOOD VESSELS:

– Subintimal fibrosis – fibrosis of the muscle wall – degeneration of internal elastic lamina – Severe narrowing of the lumen

SKIN: – Atrophic epidermis: hyperkeratosis, hyperpigmentation and hypopigmentation – Subcutaneous vessels: weakened and dilated – “Radiation dermatitis”: impaired healing, increased susceptibility to infection, ulceration

LUNGS: – Delayed radiation pneumonitis: intra-alveolar and interstitial fibrosis --> dyspnea, chronic coughand diminished lung function



KIDNEY AND URINARY BLADDER – Delayed peritubular fibrosis, vascular damage and hyalinization of glomeruli

BREAST – Radiotherapy for breast ca: dense, fibrotic reaction with extreme pleomorphism of cells

GIT – Esophagitis, gastritis, enteritis, colitis and proctitis

OVARY AND TESTIS

– Spermatogonia: suppression of meiosis and infertility – BV obliteration and fibrotic seminiferous tubules – Degeneration of ovarian follicles

EYES AND CNS – Cataracts – Damage to retinal and ciliary arteries

CNS – Focal necrosis and demyelination of white matter – Spinal cord: transverse myelitis

27. And 28. Differentiate the following and effects of deficient intake of vitamins

MARASMUS KWASHIORKOR

Depletion of somatic protein compartment Depletion of visceral protein compartment

Body weight < 60% of normal for sex,

height and age

Body weight 60% - 80% of

normal

Muscle wasting, loss of subcutaneousfat, Hypoplastic bone marrow

Edema, Hypoalbuminemia, Fatty liver

Normal or mildly decreased serumprotein “FLAKY PAINT” - Skin and Hair

OREXI ERVOS BULEMI

"a nervous loss of appetite"; “ox hunger”

self-induced starvation Binge eating and compensatory purging by

vomiting

weight drops to <85% of ideal body weight use of laxatives, diuretics, or diet pills;

exercise; or fasting.

diagnosis requires absence of menses for atleast 3 cycles

Normal weight & gonadotropin levels

refusal to maintain body weight at or above aminimal normal weight for age & height

• endocrine changes,

• nutritional deficiencies

• compensatory physiologic adaptations

• Electrolyte imbalance (ex. hypokalemia)

• Aspiration of gastric contents

• Esophageal rupture

• Chipmunk facies



28. Briefly discuss the pathogenesis of obesity.

- food-derived energy exceeds the energy expenditure

- deficiency of leptin (or obesity protein) causes an increase in production of neuropeptide Y(appetite stimulant) which increases appetite

- dysfunction of the leptin system/leptin resistance

VIT MI S EFFECTS OF DEFICIE T I T KE:

VIT. A

• NIGHT BLINDNESS

• XEROPHTHALMIA (*BITOT SPOTS-

KERATOMALACIA)

• FOLLICULAR HYPERKERATOSIS (TOAD

SKIN)

• RESPIRATORY TRACT INFECTION

• RENAL & BLADDER STONE

• IMPAIRED IMMUNITY

VIT. D

• POOR BONE MINERALIZATION

• RICKETS- overgrowth of epiphyseal plate

(Pigeon-breast deformity, Rachitic rosary,

Scoliosis, Harrion’s groove, Bowing of leg,

Frontal bossing)

• OSTEOMALACIA- derangement in bone

remodelling (osteopenia-fractures)

VIT. C

• SCURVY (INADEQUEATE OSTEOID

FORMATION) - ANEMIA RASH ANDHEMORRHAGE

NIACIN • PELLAGRA (DIARRHEA, DEMENTIA,

DERMATITIS)

FOLATE • MEGALOBLASTIC ANEMIA

• VILLOUS ATROPHY OF THE INTESTINES

RIBOFLAVIN

• CHELIOSIS

• GLOSSITIS

• PHOTOPHOBIA

• SCROTAL DERMATITIS

• ERYTHROID HYPOPLASIA

VIT B12 / COBALAMIN

• SUBACUTE COMBINED DEGENERATIONOF THE SPINAL CORD

• MEGALOBLASTIC ANEMIA

• PERNICIOUS ANEMIA

IRON • HYPOCHROMIC MICROCYTIC ANEMIA

COPPER

• MUSCLE WEAKNESS

• NEUROLOGIC DEFICITS

• HYPOPIGMENTATION

• ABNORMAL COLLAGEN X LINKING

SELENIUM • KESHAN’S DISEASE (CARDIOMYOPATHY)

ZINC• ACRODERMATITIS ENTEROPATHICA

• GROWTH RETARDATION

• INFERTILITY



29. Briefly discuss the pathogenesis and morphology the following

a. cystic fibrosis (mucoviscidosis)

- primary defect is in regulation of epithelial chloride transport leading to decreasedreabsorption of NaCl from the lumen which leads to increased sweat chloride

- in Sweat Ducts- loss of CTFR function leads to decreased reabsorption of NaCl and production of hypertonic sweat

- in Respiratory and Intestinal epithelium- loss of CTFR function result in loss or reductionof chloride secretion into the lumen while active luminal Na absorption is increased ---->

increase passive water reabsorption from the lumen -----> lowering of water content of the

surface fluid coating mucosal cells----> dehydration of lining epithelium-----> defective

mucociliary action

- Regulates transport of bicarbonates - mutant CTFR alleles secrete acidic fluids--->

decrease luminal ph ---> increase mucin precipitation----> plugging of ducts

b. hyaline membrane disease (respiratory distress syndrome in newborns)

-

c. neuroblastoma (ganglioneuroma)

- most common extracranial solid tumor in children- occur sporadically, hereditary predisposition, as abdominal masses

- 40% diagnosed in infancy and 40% occur in the adrenal medulla (most common)

- Homer-Wright pseudorosettes

30. Give the risk factors for:

a. prematurity

-> Preterm Premature Rupture of Membranes (PPROM) --30-40% of preterm deliveries,

single most common identifiable cause of prematurity

-> Intra-uterine infections- 25% of cases of preterm births; Chorioamnionitis, Funisitis – most common organisms include Ureaplasma urealyticum, Mycoplasma, G. vaginalis,

Trichomonas, GC, and Chlamydia

-> Uterine cervical and placental structural abnormalities-> Multiple gestation



b. SIDS (Sudden Infant Death Syndrome)

ainsto ming Team:

Tricia, Hannah, Jen, Powie, Khianne, JC, Abi, Klar, Angeli, DenDen, Janina, KT

Compilation:

RR, Marie

GOODLUCK 2018! To Third Year!

study guide for mss, cns

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