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STEP 1 MIXED > Deck 1 > Flashcards

Deck 1 Flashcards

1
Q

Pathogenesis huntington’s disease?

A

Transcriptional repression from huntintin protein.
INCREASED deacetylation –> silencing of genes necessary for neuronal survival
DECREASED transcription of genes needed for neuronal survival

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2
Q

What are Ladd’s bands and what do they cause?

A

Fibrous bands between retroperitnium and R colon. Crushes duodenum and causes intestinal obstruction, bilous emesis
Caused by midgut malrotation
May have volvulus

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3
Q

What is the virulence mechanism for extended spectrum beta lactamase genes?

A

Plasmids –> conjugation

Tx carbapenems

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4
Q

what is MELAS?

A 
Mitochondreal myopathy
Encephalopathy
Lactic Acidosis
Stroke
Caused by mitochondreal disorder
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5
Q

MOA and examples of Class I antiarrhythmic drugs?

A

Class I block Na+ inward current (depolarization)

Lidocaine, flacainide, procainamide

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6
Q

MOA and examples of Class II antiarrhythmic drugs?

A

B-blockers

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7
Q

MOA and examples of Class III antiarrhythmic drugs?

A

Block K+ efflux channels
used for paroxysmal afib and to maintain sinus rhythm
Prolonges repolarization
Amiodarone, dofetilide sotalol

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8
Q

MOA and examples of Class IV antiarrhythmic drugs?

A

Block L-type Ca influx channels
Slows sinus rate
Increases AV node conduction time

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9
Q

Where do T cells undergo + and - selection?

A

+ selection in thymic cortex

- selection in thymic medulla

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10
Q

What complication are patients at risk for with radical prostatectomies?

A

Erectile dysfunction

Prostatic plexus gives rise to cavernous nerves

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11
Q

MOA thiazides? Indications for use?

A

Block Na/Cl co-transporter in DCT. Increase Ca2+ reabsorption. Used in HTN + osteoporosis

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12
Q

MOA loops?

A

Block NKCC in LoH. Cause hypocalcemia

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13
Q

What is acute intermittent porphorya?

A

Autosomal dominant disease causing defective heme synthesis

PBG and ALA in urine

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14
Q

What is the enzyme missing in acute intermittne porphorya?

A

Porphobilinogen deaminase deficiency

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15
Q

Symptoms of Acute intermittent porphorya?

A

Abdo pain
neurovesicular syndrome
red urine when standing

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16
Q

Tx of AIP?

A

Intravenous heme and glucose

(ALA synthase is the rate-limiting enzyme in heme synthesis) These both inhibit heme synthesis

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17
Q

Why do hypothyroid pts get galactorrhea?

A

Lactotroph cells in hypothalamus are stimulated by TRH. Prolactin inhibits GnRH and causes amenorrhea and galactorrhea

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18
Q

What is contained in the hepatoduodenal ligament?

A

The portal triad
Hepatic artery
Portal vein
Common bile duct

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19
Q

Why is portal triad important?

A

When clamped, you can tell if bleeding is coming from one of them or from IVC/hepatic veins

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20
Q

What does aspergillus grow on? What is risk after infection?

A

Peanuts, soy, corn

Produce aflotoxin and puts you at risk for hepatocellular ca via p53 mutations

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21
Q

What will ACTH level be in 21-OH deficiency?

A

HIGH because of low cortisol levels

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22
Q

What type of disease is ILD?

A

Restrictive

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23
Q

What will lung volume loop look like for restrictive disease?

A

Shifted to R

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24
Q

What is expiratory flow like for ILD and why?

A

Increased expiratory flow due to increased radial traction (airway widening) and increased elastic recoil***

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25
Q

Longitudinal mucosal tears with vomiting. What is it? What causes it?

A

Mallory-Weiss tears caused by **increased intraabdominal pressure*

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26
Q

How does DDAVP work?

A

vWF and factor VIII increase

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27
Q

What are proteasome Tx for MM?

A

Bortezomib “boronic acid containing peptide” causing apoptosis due to accumulation of intermediates

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28
Q

What does Thyroid Peroxidase do in gland?

A

*Iodination of thyroglobulin, *coupling of iodized tyrosine, and *oxidation of iodid

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29
Q

What determines blood flow to heart? (main factor)

A

Duration of diastole

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30
Q

What are segmented viruses? What is significance of them being segmented?

A 
Can undergo reassortment and antigenic shift/drift
Rotavirus
Reovirus
Orthomyxovirus
Arenavirus
Bunyavirus
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31
Q

MOA ethosuxamide?

A

Decrease Ca2+ channels in thalamus

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32
Q

What are the antiepileptics blocking Na+?

A

Valproic acid, carbamazepine, phenytoin

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33
Q

How do you get silicosis?

A

Industrial exposure to coal and sand

34
Q

What do you see on histology of silicosis?

A

Collangeous nodues with dust laden macrophages. Interstitial collagen deposition
Round nodules in upper lobes w eggshel calcifications

35
Q

MOA colchicine?

A

Inhibit Microtubular polymerization
Inhibit phagocytosis, chemotaxis, degeneration
Used in pts who can’t take NSAIDS

36
Q

What enzyme deficiency causes SCID?

A

Adenosine deaminase deficiency (lymphotoxicity)

37
Q

What is the MOA for mycophenolate and ribavirin?

A

Inhibit IMP dehydrogenase (inosine mono phosphate dehydrogenase). Inhibits purine synthesis in T cells and

38
Q

What is caused by HGPRT deficiency?

A

Lesh Nyhan. Increased Uric Acid production

39
Q

Why can’t you give 6-mercaptopurine and azothioprine together?

A

6 mercaptopurine binds PRPP in purine pathway and causes T-cell toxicity. It’s metabolized by xanthine oxidase so you can’t give azothioprine unless clinically indicated

40
Q

What two factors are needed to grow H influenzae?

A

NAD+ and hematin (Factors V and X). H influenzae will grow if plated with staph because it has NAD+

41
Q

Infant with large fontanelle, protruding tongue, umbilical hernia, dry skin, jaundice. What is it?

A

Congenital hypothyroidism

42
Q

Danger of congenital hypothyroidism?

A

Permanent intellectual disability

43
Q

What are brain changes in Huntington’s Disease? What receptors are activated?

A

Degeneration of caudate nuclus and putamen. Binding NMDA receptors bind glutamate and cause neuronal death

44
Q

What are stages of lobar pneumonia and what cells are involved?

A

Congestion - pronteinateous fluid and leaky cappilaries
Red hepatization - liver like, neutrophils, fibrin, erythrocytes
Grey hepatization - macrophages
Resolution - macrophages

45
Q

Embryology of the pancreas?

A

Ventral and dorsal buds fuse at 8 weeks
Ventral becomes part of head and main duct
Dorsal becomes everything else (majority – superior head, body, tail) + accessory duct

46
Q

What is FMD?

A

Non-atherosclerotic disease affecting arteries. Fibromuscular webs & aneurysms
*Absent internal elastic lamina
String-on-bead appearances
Affects cerebrovasculature and kidneys. RAS and aneurysms

47
Q

MOA arsenic poisoning? Where is it found?

A

Inhibits cellular respiration, gluconeogenesis, and glutathione metabolism
Binds to sulfhydryl groups

Found in insecticides & contaminated water

48
Q

Presentation arsenic poisoning?

A

**severe watery diarrhea
Garlic breath
Hypotension
Chronic: hyperkeratosis, abnormal pigmentation, glove in stocking neuropathy

49
Q

Tx arsenic poisoning?

A

Dimercaprol inhibits arsenic binding sulfhydryl groups

50
Q

How does methyltestosterone (androgen steroids) cause comedomal acne?

A

Excessive follicular epidermal hyperproliferation and sebum production

51
Q

What medications cause tardive dyskinesia?

A

Dopamine antagonists

Antipsychotics, metclopramide

52
Q

Benefits and risks of selective COX 2 inhibitors?

A

Benefits: anti-inflammatory effects, less bleeding risk, no gastric uceration
Risks: Increased thrombotic and cardiovascular events due to inhibition of prostacyclins (vasodilators and antigoagulant)

53
Q

Test for sickle cell trait?

A

Hb electrophoresis

54
Q

SE doxorubicin?

A

Dilated cardiomyopathy

55
Q

MOA Anthracyclines?

A

Anthracyclines (doxorubicin, donorubicin) bin Topoisomerase II and create structures that break DNA. Also create free radicals and iron-complexes that cause cardiotoxicity

56
Q

What agent should be administered along with doxorubicin?

A

Dexrazoxane- chelating agent blocking the formation of iron-containing complexes and binding of topoisomerase II in healthy cardiac myocytes.

57
Q

Which substances cause gastric acid secretion in parietal cells?

A

Histamine, Ach, gastrin

58
Q

What is systemic mastocytosis?

A

Mast cell degranulation resulting from KIT receptor tyorsine kinase mutations.
Urticaria, puritis, hypotension, flushing, increased gastric acid secretion from histamine release**

59
Q

What is zenker diverticulum caused by?

A

Cricopharyngeal motor dysfunction and oropharyngeal dysphagia

60
Q

What does activation of muscurinic receptors do?

A

Vasodilation by production of NO, smooth muscle relaxation

Also detreusor muscle contraction, increased parystalsis, pupillary constriction

61
Q

MOA muscurinic receptors causing smooth muscle relaxation?

A

increase in cGMP causing myosin light chain to activate phosphatase–> inhibits myosin and actin from binding

62
Q

What are integrins? What do they bind?

A

Transmembrane receptors that bind extracellular matrix or other cells. Fibronectin, collagen, laminin. Gets downregulated in melanoma

63
Q

What are effects of glucocorticoids on liver?

A

Increased gluconeogenesis and glycogenesis. Insulin antagonism –> hyperglycemia

64
Q

How does acoustic neuroma present?

A

Unilateral hearing loss + tinnitus

65
Q

Where does food aspirate when supine vs standing?

A

Supine- posterior segments of upper lobes, superior segments of lower lobes

Standing- basilar segments of lower lobes
“Swallow a bite, goes down the right”

66
Q

Which rib overlies R kidney?

A

12th rib

67
Q

What is Type I error? What is alpha?

A

Type I error is when researchers fail to accept the null hypothesis when the null is really true

Alpha = percent chance that the researchers are willing to risk Type I error. Set at 0.05 like p

68
Q

What is Type II error? What is Beta?

A

Type II error = researchers fail to reject the null hypothesis even though the null is truly false.

Beta = chance of making a Type II error.

69
Q

What is 1-beta in statistics?

A

Statistical Power = study’s ability to detect a difference when it exists. Probability of rejecting the null when it is truly fase (finding a true relationship). Depends on sample size and difference in outcome between groups being tested

70
Q

How does latanoprost work?

A

Glaucoma med. Prostaglandin analogue– increases uveoscleral and aqueous humor outflow

71
Q

How does dorzolamide work?

A

Glaucoma med, CA inhibitor. Decreases bicarb production in ciliary body and decreases acqueous production

72
Q

How is Ca2+ removed from cell in the final stage of myocyte contraction?

A

Via Na/Ca+ exchanger and Ca+ ATPase. Brings the Ca back to SR or out of cell

73
Q

What part of the brain produces norepinephrine? What does this part of the brain do?

A

Locus cerulius- Posterior rostral pons near floor of 4th ventricle

Responsible for sleep, arousal, consciousness (reticular activating system), cognition, BP control

74
Q

How does digoxin work?

A

Inhibits Na/K ATPase. Inhibits Na efflux and inhibits Ca efflux

75
Q

What shows on histology with HIV dementia?

A

Microglial nodules with multinucleated giant cells

76
Q

Where does isotype switching occur?

A

Germinal centers, must activate CD40

77
Q

What is primary and secondary immune response from B cells?

A

IgM, then isotype switching, then secondary response is IgG

78
Q

Who gets Giardia infections?

A

People with IgA deficiency

79
Q

What are symptoms of IgA deficiency?

A

Recurrent sinopulmonary infections, GI infections (Giardia), coeliac disease, anaphylactic blood transfusion reaction,

80
Q

How does HIV-2 present?

A

Longer asymptomatic periods, labs won’t show HIV-1 viral levels even when symptomatic, lower levels of viremia

Endemic to West Africa (senegal)

STEP 1 MIXED (13 decks)

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