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Test 11 Flashcards

1
Q

What is the main toxin produced by C. perfringens? What is it’s function?

A

Alpha toxin (lecithinase= phospholipase C)

Lecithinase degrades lecithin (component of cell phospholipid membranes) that leads to cell destruction NECROSIS (gas gangrene) and hemolysis.

PERFringens PERForates a gangenous leg with alpha toxin.

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2
Q

Why does c. perfringens produce gas?

A

It uses carbs for energy–the rapid metabolism of muscle tissue produces gas that can be seen on xray or CT.

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3
Q

What are the three plasminogen activators?

A

streptokinase (Exotoxin released by S. Pygoenes)
urokinase
TPA

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4
Q

What is one of the most common reasons for elevated AFP levels?

A

underestimation of gestational age, confirmed by fetal US

*fetal liver, GI tract and yolk sac= source

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5
Q

What are other reasons for elevated AFP?

A
  1. Neural tube defects
  2. Anterior abdominal wall defects (omphalocele, gastroschisis)
  3. Multiple gestation
  4. Down Syndrome
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6
Q

What are decreased estriol levels indicative of?

A

Placental insufficiency

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7
Q

What are INCREASED levels of hCG (synth from trophoblastic tissue) associated with?

A

multiple gestation
hydatiform mole
choriocarcinoma

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8
Q

What is a mitochondrial enzyme that activates caspases and indirectly brings about cell death through intrinsic pathway apoptosis?

A

Cyt C

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9
Q

What is Edwards Syndrome?

A

47 xx +18 (nondisjunction)

Small jaws
small eyes
low formed ears
rocker bottom feet  (also in Patau)
CLENCHED HANDS W/ OVERLAPPING FINGERS**
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10
Q

Flat face, abnormal ears, slanted palpebral fissures, redundant neck skin, single transverse palmar crease are associated with what genetic disorder?

A

Down syndrome

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11
Q

Cleft lip and palate, polydactyly and omphalocele are associated with what genetic disorder?

A

Patau syndrome

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12
Q

Tall male w/ gynecomastia and infertility is indicative of…

A

Klinefelter syndrome (47XXY)

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13
Q

An inability to normally metabolize fat is indicative of…

A

exocrine pancreatic insufficiency

Often from alcholism

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14
Q

What cytokines down regulate local inflammation?

A

TGF-B

IL-10

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15
Q

Do advance directives take precedence over wishes of family members?

A

Yes

Physicians should adhere to patient’s wishes outlined in advance directives

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16
Q

What is the most prevalent collagen in the human body?

A

Type I

Bone
Skin
Tendon

LATE wound repair

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17
Q

What type of collagen is associated w/ osteogenesis imperfecta?

A

type I

easily fracturable bones

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18
Q

What is made of type II collagen?

A 
carTWOLage (hyaline)
vitreous body (jelly in eye)
nuclous pulposus (jelly in spine)
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19
Q

What is made of type III collagen?

A 
Reticulin
skin
blood vessels
uterus
fetal tissue
granulation tissue
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20
Q

What is deficient in ED syndrome?

A

type III collagen

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21
Q

What is made of type IV collagen?

A

Basement membranes
basal lamina
lens

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22
Q

What is defective in alport syndrome?

A

type IV collagen

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23
Q

What is targeted by autoantibodies in Good pasture syndrome?

A

type IV collagen

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24
Q

Pain sensation from the mediastinal/diaphragmatic parietal pleura is carried by what nerve?

A

phrenic

C3, 4, 5

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25
Q

Damage to what nerve causes a winged scapula?

A

long thoracic

serratus anterior

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26
Q

What is the CFTR protein?

A

Transmembrane ATP gated Cl channel

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27
Q

What causes CF?

A

Mutation in the CFTR gene on chromosome 7

AR disease

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28
Q

What is the agent of choice for prevention and tx of post-MI arrythmias?

A

Lidocaine

Binds depolarizing and depolarized cells–> ISCHEMIC myocardium is depolarized tissue

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29
Q

What are class IB antiarrythmics?

A

Little Mexican w/ an M

Lidocaine
MEXiletine

Decreases AP

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30
Q

What antiarrythmic is used to treat re-entrant or ectopic SVT/VT?

A

Class IA

QDP:
Quinidine
Procainamide
Disopyramide

Increases AP/ERP/QT

31
Q

What antiarrythmic causes cinchonism?

A

1A: QDP

32
Q

What antiarrythmics are often used to treat SVTs like a. fib?

A

1C: FP
Flecainide
Propafenone

Increase ERP in AV node and accessory bypass tracts
doesn’t affect AP duration

33
Q

What drugs are CONtraindicated in isCHEMIC heart disease?

A

1C: Flecainide, Propafenone

34
Q

What drugs help control ventricular rate and are used for a. fib and a flutter?

A

Class I (Beta blockers)

Decrease SA/AV nod by decreasing cAMP /Ca currents

*decrease the slope of phase 4

35
Q

What drug is especially good for v. TAch?

A

Class II (AIDS)

Amiodarone (specifically)
Ibutilide
Dofetilide
Sotalol

Increased AP, ERP, QT–> prolonged repolarization

36
Q

What beta blockers are good for TDPs?

A

Sotalol

Ibuitilide

37
Q

What class III antiarrythmic can affect the lung, liver and thyroid and lead to blue/gray skin deposits?

A

Amiodarone

38
Q

What drugs are used to prevent nodal arrhythmias (SVT)?

A

Class IV: Verapamil, diltiazem

Decrease conduction velocity, increase ERP, PR

Blocks Ca channels> slows depol in phase 0 and latter part of phase 4> slows rate of SA node firing and AV node conduction

39
Q

What antiarrythmic causes constipation, flushing , edema, HF?

A

IV: VP

40
Q

What is the drug of choice for supraventricular tachycardia?

A

Adenosine (increases K out of cell> hyperpolarizing cell> decraese Ca)

41
Q

What is digoxin used for?

A

A. Fib

slows conduction through AV node

42
Q

What electrolyte abnormalities are seen in a pts with primary adrenal insufficiency (Addisons)?

A

Decreased aldosterone> decreased reabsorption Na> decreased excretion of K and H

  1. Hyponatremia
  2. Hyperkalemia
  3. Met acidosis> low serum bicarb> compensatory incrase in Cl
  4. Hypercholremia
43
Q

What is the most effective way to provide long term relief to pts with PUD?

A

Eradicate H. pylori using Antibiotics

44
Q

Ranitidine

A

H2 blockers> decreased H secretion by parietal cells

45
Q

Sucralfate

A

Binds to base of mucosal ulcers and protectsa gainst gastric acid allwoing ulcers to heal

46
Q

Metoclopramide

A

DA antagonist> increases resting tone, LES tone, motility

Diabetic and postsurgery gastroparesis

Antiemetic

47
Q

Misoprostol

A

PGE1 analog

Prevents NSAID induced ulcer disease

48
Q

How does CO affect O2 binding on heme iron?

A

CO binds to Hb w/ 220 times the affinity of O2 for Hb leading to Carboxyhemoglobin. This causes a left shift and a decreased in O2 binding capacity as well as deficient unloading of O2.

tx: 100 O2 and hyperbaric O2

49
Q

Night blindness, xeropthalmia, vulnerability to infection (measoles)

A

vit A

50
Q

Cheilosis, corneal vascularization

A

Vit B2

51
Q

Cheilosis and periopheral neuorpathy

A

B6

52
Q

Pellagra

A

Niacin (dermatitis, dementia, diarrhea)

53
Q

Scurvy, impaired wound healing

A

Vit C

54
Q

Pernicious anemia

A

B 12

55
Q

What syndrome is characterized by low plasma Na and osmolality, concentrated urine and increased urine Na volume, but NORMAL extracellular fluid volume?

A

SIADH

56
Q

What is an important cause of SIADH?

A

paraneoplastic effect secondary to small cell lung cancer

57
Q

What is the power of a study?

A

The ability of a study to detect a difference between groups when a difference really exists. Related to type II error (not an effect when one exists)

P= 1-B (B is type II error rate)

58
Q

Where are receptors for cortisol located?

A

In the cytoplasm, then translocate to the nucleus

59
Q

Receptor for insulin?

A

cell surface receptor> activation TK> suppression gluconeogenesis

60
Q

Receptor for GH?

A

memberane bound Jak/STAT> increased gluconeogenesis

61
Q

Receptor for NE/EPI/Glucagon?

A

GPCR membrane receptors> increases cAMP> AC> increase glycogenolysis

62
Q

What causes meningoencephalitis in HIV + patients?

A

Cryptococcus neoformas

Inhalation> hematogneous dissemination to meninges

63
Q

What is used for dx of c. neoformas?

A

latex agglutination detects the polysaccharide capsule Ag of Cryptoccus

INDIA INK shows ROUND/OVAL unequal budding yeast

64
Q

Nonspetate hyphae that branch at wide angles

A

Mucor and Rhizopus

cause infection of paranasal sinuses in immunosuppressed

65
Q

Germ tubes (sprouts of true hyphae from yeast cells)

A

Candida

66
Q

Spherules

A

Tissue form of Coccidiomycosis

67
Q

What is the neurotoxin released by C. Tetani?

A

Tetanospasm> exotoxin> tetanus

Block release of inhibitory interneurons in spinal cord that use GABA and glycine as their NT> prevents release of NT> spastic paralysis

68
Q

What causes flaccid paralysis?

A

C. Botulinum> releases pre-formed heat labile toxin that inhibits ACh at NM jxn> flaccid paralysis

69
Q

What is the mechanism of penicillins and cephalosporins?

A

Irreversibly bind to PBPs (transpeptidases)

70
Q

Where does Vancomycin bind

A

Terminal D alanine residues of CELL WALL glycoproteins preventing transpeptidases from forming cross links

71
Q

What is the mechanism of fluoroquinolones?

A

bind to proteins like DNA gyrase > interfere w/ DNA replication

72
Q

What is a mechanism of resistance to ceophalosporins?

A

Change in PBP structure

73
Q

How do corticosteroids affect a CBC?

A

Corticosteroids lead to dermarginalization of neutrophils that were previously attached to a vessel wall> increased neutrophils

Decreased: lymphocyte, monocyte, basophil and eosinophil

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