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Test reviews DEDICATED > Day 4 June 24 > Flashcards

Day 4 June 24 Flashcards

1
Q

Is asthma mediated by a Th1 or Th2 response?

A

Th2

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2
Q

Role of Th1 response?

A

Cell mediated adaptive immunity (targeting intracellular pathogens)
-type IV sensitivity reactions

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3
Q

Is a th1 or th2 response implicated in a type IV hypersensitivity reaction?

A

Th1

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4
Q

What is the function of IL5?

A

recruits eosinophils

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5
Q

which two cytokines are secreted by Th2 cells to stimulate B cell class switching to igE (in asthma)?

A

IL4 and IL13

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6
Q

anticentromere antibodies are found in which conditions?

A 
CREST 
Calcinosis
Raynauds
Esophageal dysmotility
Sclerodactyly
Telangiectasias
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7
Q

Which autoantibodies is SPECIFIC for rheumatoid arthritis?

A

anti-cyclic citrullinated peptide (anti-ccp)

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8
Q

why are anti-cyclic citrullinated protein antibodies found in RA?

A

tissue inflammation leads to arginine residues in proteins to be converted to cirtulline, this alters the shape and can generate an immune response

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9
Q

Phosphatidylcholine AKA

A

lecithin

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10
Q

how does the Phosphatidylcholine : sphinomyelin ratio change throughout pregnancy?

A

The ratio is about equal until the middle of the third trimester, when phosphatidylcholine increases sharply as type II pneumocytes have begun secreting surfactant

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11
Q

What lecithin to sphinomyelin ratio indicates adequate surfactant production to prevent hyaline membrane disease in the neonate?

A

2:1

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12
Q

Most common lead point for intussusception?

A

ileocolic junction -difference in sizes allows to small bowel to go into large bowel

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13
Q

Clinical presentation of intussusception?

A

colicky pain, nausea, vomiting and currant jelly stools

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14
Q

what type of hormone is ADH?

A

peptide

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15
Q

what type of hormone is prolactin?

A

peptide

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16
Q

what vitamin is essential for NAD and NADP?

A

B3 (nicotinic acid)

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17
Q

what causes niacin deficiency in developing countries? in developed countries?

A

Corn diet

Poor nutrition

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18
Q

niacin may be synthesized from ___

A

tryptophan

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19
Q

Serotonin may be synthesized from ___

A

tryptophan

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20
Q

tyrosine can be synthesized from ___

A

phenylalanine

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21
Q

DOPA, dopamine, NE and epinephrine are synthesized from….

A

tyrosine (which comes from phenylalanine)

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22
Q

Presentation of inhalant abuse?

A

transient euphoria, lethargy, disorientation, LOC, poor coordination, slurred speech - short duration of effects-rapid recovery
-‘glue sniffers rash’ - dermatitis around mouth or nose

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23
Q

what mutation is commonly found in patients with familial dilated cardiomyopathy?

A

TTN -a truncating mutation of titin - the protein that anchors myosin heavy chains to Z discs in the sarcomere

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24
Q

inheritance of TTN mutation?

A

autosomal dominant, with incomplete penetrance - meanign it may show up later in life or not at all

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25
Q

presentation of dilated cardiomyopathy

A

symptoms of decompensated heart failure possibly resulting in sudden cardiac death from arrhythmia

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26
Q

which genes are commonly mutated in patients with hypertrophic cardiomyopathy?

A

Beta myosin heavy chain or myosin binding protein C mutations

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27
Q

a mid shaft humeral fracture may damage which structures?

A

radial nerve -loss of extension of hand/elbow and loss of supination
deep brachial artery

28
Q

acyclovir MOA

A

guanosine analog - HSV phosphorylates it into its active form which them impairs DNA polymerase mediated replication

29
Q

why is acyclovir not as active in EMV or CMV?

A

these virus’s dont have the same thymidine kinase as HSV and thus do not phosphorylate the drug into its active form

30
Q

how may body composition change after taking highly-active antiretroviral therapy (HAART)?

A

Lipoatrophy in the face, extremities and buttocks with central fat deposition causes increased abdominal girth and buffalo hump

31
Q

MOA of thiazolidinediones?

A

bind to and activate PPAR gamma

32
Q

PPAR gamma MOA

A

upregulates genes resulting in increased GLUT4 ->

  • increased glucose uptake in adipose and skeletal muscle in response to insulin
  • increased adiponectin - sensitives adipose cells to insulin and stimulates FFA oxidation
33
Q

what drugs can cause methemoglobinemia?

A
  • Dapsone
  • Nitrites/nitrates
  • Local/topical anesthetics (benzocaine, teething medications)
34
Q

Presentation of methemoglobinemia?

A

Cyanosis
Chocolate-brown blood
Innacurate pulse oximetry

35
Q

Management of methemoglobinemia

A

Meythlyne blue -reduces iron back to Fe2+

36
Q

In which layer are parietal cells found?

A

The upper glandular layer

37
Q

In which layer are cheif and delta cells found?

A

deep gastric glands

38
Q

how does vagal stimulation increase H release int he stomach?

A

Causes Ach secretion, which binds to M3, which activates Gq -> IP3 and increased Ca, activates H/K pump

39
Q

How does gastrin increase H release in the stomach?

A

Binds to CCKb receptor ->activates Gq -> increasd IP3 and Ca -> activation of H/K pump

40
Q

how does histamine increase H release in the stomach?

A

binds to H2 receptor -> activates Gs -> increase cAMP -> activation of H/K pump

41
Q

how do prostaglandins and somatostatin decrease H secretion in the stomach?

A

bind to their receptors and activate Gi -> decreased cAMP -> decreased H/K activity

42
Q

how does mitochondrial myopathy present?

A

Brain and muscle effected first due to high metabolic demand - > muscle weakness, myalgia, lactic acidosis, nervous system dysfuction (seizures, neuropathy)

43
Q

what will be seen on muscle biopsy of someone with mitochondrial myopathy?

A

ragged red fibers

44
Q

medication induced esophagitis is associated with which type of drug?

A

bisphosphonates

45
Q

bisphosphonates MOA?

A

inhibits osteoclasts

46
Q

osteonecrosis of the jaw is associated with what drugs?

A

bisphosphonates

47
Q

how are monoclonal antibodies eliminated?

A
  1. Target mediated drug clearance- internalized via receptor mediated endocytosis
  2. Non specific clearance: taking up by reticuloendothelial cells and vascular endothelial cells
48
Q

are monoclonal antibodies eliminated in the liver or kidney?

A

NOOOOOOOO

49
Q

how does impaired beta oxidation present?

A

hypoketotic hypoglycemia -presents after a significant fast leading to hypoglycemia, hepatomegaly, and liver dysfunction

50
Q

what does a deficiency of acyl - coa synthase cause?

A

primary carnitine deficiency (this is a deficiency of transporting LCFAs into the mitochondria, leading to toxic accumulation)

51
Q

name two disorders of beta oxidation

A

MCAD deficiency

Primary carnitine deficiency

52
Q

what is MCAD caused by?

A

deficiency in medium chain acyl-coA dehydrogenase - > cant break down fatty acids into acetyl-coa

53
Q

presentation of MCAD deficiency?

A

Hypoketotic hypoglycemia, seizures, vomiting, lethargy, coma, liver dysfunction, hyperammonia, can cause sudden death in infants and children

54
Q

how to treat disorders of beta oxidation?

A

avoid fasting

55
Q

explain the membrane physiology of pacemaker cells (nodal cardiac cells)

A

Theres only phase 0, 3 and 4

0: upstroke - L type Ca channels open at -40, leading to Ca influx
3: repolarization - closure of L type Ca channels, and efflux of K channels
4: pacemaker potential - slow influx of Na, with slow decrease of K efflux. When the membrane gets to -50, T type Ca channels open, then at -40, L type open -> depolarization

56
Q

Which phase of the cadiac nodal action potential does adenosine and acetylcholine effect?

A

Phase 4

57
Q

Effects of adenosine on phase 4 of the myocardial action potential in nodal cells (MOA)

A
  • increase the efflux of K by binding A1 receptors and inhibits L-type Ca channels decrease influx
  • this results in the cell staying negative and increases the time between depolarizations - slowed sinus rate
58
Q

Cardiac use of adenosine

A

terminating paroxysmal supraventricular tachycardia

59
Q

which nerve originates from the musculocutaneous nerve?

A

the lateral cutaneous nerve of the forearm - sensory to lateral forearm

60
Q

pathophys of post strep glomerulonephritis

A

immune complex deposition along the basement membrane of the glomerulus (deposits of igG, igM, and c3

61
Q

is post strep glomerulonephritis a nephritic or nephrotic syndrome?

A

nephRITIC

62
Q

what does post strep glomerulonephritis look like on electron microscopy?

A

dome shaped subepithelial humps

LUMPY BUMPY

63
Q

Fibrin deposition is characteristic of which nephritic syndrome?

A

rapidly progressive (crescenteric) glomerulonephritis

64
Q

why is dextrose useful for treating an attack of AIP?

A

IV dextrose = carb loading

and glucose inhibits ALA synthase

65
Q

how does carbamazepine?

A

inhibits Na channels preventing recovery from inactivation -decreased nerve firing rate

Test reviews DEDICATED (70 decks)

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