Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Daily Flashcard Quizzes > 7/15 > Flashcards

7/15 Flashcards

1
Q

what is a major determinant of viral tropism with enveloped viruses

A

the extent to which the viral surface proteins can bind to complementary host cell plasma receptors

depends on the viral envelope glycoprotein and its affinity for the host cell surface glycoproteins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

what are standard precautions for C diff

A

wash with soap and water

gown
non sterile gloves

(masks are for droplet precautions)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

what is a type 1 vs type 2 error

A

Type 1/alpha:
falsely concluding there’s a difference
“falsely thinking you’re number 1”

Type 2/beta:
falsely concluding there is no different
“falsely thinking being 2nd best is ok”

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

what is Berkson’s bias

A

selection bias when you’re selecting hospitalized (sick) pts as your control group

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

what are asplenic pts at risk for

A 
infection with encapsulated bacteria
SHiN
Strep pneumo
Haemophilus Influenzae 
Neisseria
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

what does the spleen do that asplenic pts are missing out on

A

spleen does 2 things:

acts as a blood filter capable of removing circulating pathogens

acts as a major site of opsonizing antibody synthesis

you could describe that as “systemic bacterial clearance”

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

what is the problem in CGD

A

susceptibility to catalase-positive organisms

they can be phagocytksed but cannot be killed effectively w/o NADPH oxidase.

“defective intracellular killing”

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

where is complement produced

A

liver

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

what is immediate hypersensitivity

A

results from IgE-mediated mast cell degranulation

“imEEEdiate”

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

what is the only fungus that has a polysaccharide capsule

A

cryptococcus neoformans

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

what organism pairs with the ‘Micicarmine stain” buzzword

A

cryptococcus neoformans

it appears red on this stain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

what is reaction formation

A

taking negative thoughts/feelings and doing the exact opposite

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

what is splitting

A

see something as “all good” or “all bad”

often with a borderline personality disorder

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

what is somatic symptom disorder

A

extreme preoccupation with unexplained medical symptoms and excessive health care use

symptoms are not intentional

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

how do you best treat somatic symptom disorder

A

schedule regular visits with the same provider

limit unnecessary workup and referral to specialists

reassure that a serious illness has been ruled out

legitimatize symptoms but focus on functional improvement as the treatment goal, rather than symptom-driven visits

  • decrease stress
  • improve coping strategies
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

distinguish Tourette syndrome from Chronic Tic disorder

A

Tourette:
motor AND vocal tics > 1 yr
(characteristically wax and wane)

Chronic tic disorder:
motor OR vocal tics > 1 yr

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

what is a t-test for

A

compare difference between the means of 2 groups

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

what is Analysis of Variance for

A

ANOVA:
compares the difference between the means of 2 or more groups

ALL quantitative variables

“ANOVA = 3 words”

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

what is a Chi square test for

A

used to evaluate the association between 2 categorical variables

ALL qualitative variables

“chi-tegorical”

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

what are anti-Smith antibodies specific for

A

SLE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

what are anti-Smith antibodies’ target

A

autoantibodies against snRNPs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

what can a SLE pt with anti-Smith antibodies not do

A

remove introns from RNA transcripts

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

what is wet and dry beriberi

A

2/2 thiamine deficiency

dry:
bilateral peripheral neuropathy

wet:
neuropathy + CHF

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

what is B6 deficiency characterized by

A

cheilosis, glossitis, dermatitis, affective symptoms (irritability)
sideroblastic anemias

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

what does Thiamine used for

A

cofactor in several synthesis steps: “ATP”:
alpha-ketoglutarate dehydrogenase (TCA cycle)
Transketolase (HMP shunt)
Pyruvate dehydrogenase (links glycolysis to TCA cycle)

also branched-chain alpha-ketoacid dehydrogenase (in Maple syrup urine disease)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

how does colchicine help in gout

A

binds and stabilizes tubulin to inhibit microtubule polymerization, which will impair NEUTROPHIL chemotaxis and degranulation

acute and prophylactic value

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

what is the bruising process

A

the purple/blue color of a bruise is RBCs (with Hb) escaping into the tissue

RBC destruction causes the release of iron-containing heme molecules

HEME OXYGENASE (in macrophages) degrades heme into Biliverdin, CO, and Ferrous iron

BILIVERDIN IS GREEN! (verde)

Biliverdin is further reduced to
bilirubin

BILIRUBIN IS YELLOW! when transported to the liver bound to albumin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

what suggests a general nephritic syndrome

A

HTN, hematuria, and moderate proteinuria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

what are linear deposits made of on renal biopsy, and what are they characteristic of

A

mad elf IgG and C3

anti-glomerular BM disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

what are the different immunofluorescent findings in RPGN

A

linear:
anti-BM antibody
Goodpasture syndrome

Granular:
PSGN
or diffuse proliferative GN in SLE!

Negative:
pauci-immune, so you have ANCA’s
C-ANCA: Wegener’s
P-ANCA: microscopic polyangiitis or Churg-Strauss

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

what is the characteristic renal pathology in a lupus pt? 2nd most likely?

A

Diffuse proliferative glomerulonephritis!!!

or if it’s nephrotic,
Membranous Glomerulonephritis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

how do you differentiate between Goodpasture and Wegener

A

Goodpasture:
lung
kidney
linear IF (anti-GBM)

Wegener:
"C disease"
Nasopharynx!!!
lung
kidney
c-ANCA (negative IF)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

how do you differentiate between Churg-Strauss and Microscopic Polyangiitis

A

both are p-ANCA (with negative IF)
both are micro-vasculitides

Churg Strauss:
granulomatous inflammation
eosinophilia!!
asthma

Microscopic polyangiitis:
presents similarly to Wegener disease (C disease), but without c-ANCA and without nasopharynx involvement

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

what do you see on membranoproliferazive glomerulonephritis

A

BM splitting (tram tracking!!) on light microscopy using PAS stains

glomeruli are lobular with proliferating mesangial cells and increased mesangial matrix.

Granular deposits on IF (lumpy bumpy)

type 1 is sub epithelial
type 2 is intramembranous

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

which 2 renal diseases have effacement of podocyte foot processes

A

minimal change disease

focal segmental glomerulonephritis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

which 2 renal pathologies have immune complex deposition giving a granular IF

A

membranous nephropathy

membranoproliferazive glomerulonephritis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

which 2 renal pathologies are 2/2 systemic disease that affect glomeruli

A

Diabetes

systemic amyloidosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

what are Kimmelstiel-Wilson nodules a buzzword for

A

diabetic nephropathy

they’re nodules of sclerosis within the glomeruli

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

which cancer is Minimal change disease associated with

A

Hodgkin Lymphoma

Reid Sternberg cells produce massive cytokines

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

which renal pathology gives you spike and dome appearance on EM

A

membranous nephropathy

thick membranes + immune complex deposition

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

what diseases are membranous nephropathy associated with

A

Hepatitis B,C

SLE if it’s not Diffuse proliferative glomerulonephritis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

how do you identify systemic sclerosis affecting kidneys

A

apple-green birefringence with Congo Red staining 2/2 amyloid deposits!!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

what stain apple-green with congo-red stain

A

Amyloidosis!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

what is Berger disease

A

AKA IgA nephropathy!

IgA immune complex deposition in mesangium

commonly in childhood
with RBC casts
following mucosal infection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

what can IgA nephropathy be associated with

A

Henoch Schonlein Purpura!!!
with palpable purpora on buttocks, arthralgia, GI pain 2/2 URI commonly

both have IgA deposition

46
Q

what is Alport syndrome

A

inherited defect in type 4 collagen (on the floor)

Albert:
“can’t see, can’t pee, can’t hear a bee while he basket-weaves!”

retinopathy/lens dislocation
glomerulonephritis
sensorineural deafness
basket-weave appearance on EM

47
Q

what is the AR equation and the ARR equation, and which NNT/NNH does each pair with

A

AR = (a / a+b) - (c / c+d)
pairs with NNH (1/AR)

ARR = (c / c+d) - (a / a+b)
pairs with NNT (1/ARR)

extra R = “reverse” alphabet;

48
Q

what is NNH equation and the NNT equation

A

NNH = 1 / AR

NNT = 1/ARR

49
Q

how can you accelerate fetal lung development in a pregnant mom expecting a preterm baby

A

Betamethasone or Dexamethasone is administered to pregnant women at risk for premature delivery to prevent neonatal ARDS.

they have the greatest efficacy in increasing surfactant production by accelerating the maturation of type 2 pneumocytes

50
Q

what is the rapid treatment option for RA relief

A

NSAIDs and glucocorticoids help provide immediate, short-term relief

51
Q

what can a pt with anti-phospholipid antibodies have

A

pt has SLE

52
Q

what do anti-phospholipid antibodies do

A

can cause a paradoxical prolongation of PTT and a false-positive RPR/VDRL (syphilis) test

pts with anti-phospholipid antibodies are at risk for venous and arterial thromboembolisms and recurrent, unexplained pregnancy losses

53
Q

how long does it take to lose cardiomyocyte contractility after onset of total ischemia

A

60 seconds

if the ischemia lasts less than 30min, restoration of blood flow leads to reversible contractile dysfunction (myocardial stunning), with contractility gradually returning over several hours/days.

after 30min of total ischemia, ischemic injury becomes irreversible

54
Q

what is Hyper-IgM syndrome

A 
defect in CD40L Ligand on Th cells,
leading to class switching defect on B cells

Findings:
high IgM
low of everything else
“defective signaling between activated CD4 T cells and B lymphocytes

55
Q

what immunoglobulins are on naive B cells

A

IgM and IgD prior to activation

this is why a hyper-IgM pt with defect in CD40L can still produce an IgM response

56
Q

distinguish transference and displacement

A

transference:
pt projects feelings about formative or other important persons onto physician (doctor is seen as their bad parent)

displacement:
transferring avoided ideas and feelings to a safer person (mother yells at her child because her husband yelled at her)

57
Q

distinguish Type 1 from Type 2 muscle fibers

A 
Type 1:
slow twitch; red
high mito and myogolbulin (high oxidative phosphorylation) for sustained contraction
increases with endurance training
"1 slow red ox" (posture muscles)

Type 2:
fast twitch; white
low mito and myoglobulin (high anaerobic glycolysis)
increases with weight/resistance training

58
Q

why are skeletal muscles not affected by CCBs

A

skeletal muscles rely on mechanical RyR calcium channels to release Ca from the SR. it does not require Ca influx across its cell membrane to work

59
Q

which lymphocytes are seen in the peripheral blood smears of pts with EBV

A

activated CD8+ cytotoxic T cells

they function to destroy virally-infected B-lymphocytes.

they are very large, and irregularly shaped, conforming to the borders of neighboring cells

60
Q

what are the 4 types of hypersensitivity reactions

A

Type 1:
Immediate:
anaphylaxis, allergies
preformed antibodies

Type 2:
Cytotoxic
antibody mediated

Type 3:
Immune complex mediated

Type 4:
delayed type

"ACID"
Anaphylaxis
Cy-two-toxic
Immune complex mediated
Delayed
61
Q

Run through Type 1 hypersensitivity rxn

A

Immediate

Humoral: IgE

Cellular: Basophils, mast cells

Anaphylaxis, Allergies

IgE is on presensitized mast cells and basophils, triggering an immediate release of vasoactive amines that act at poastcapillary venues (histamine).
Rxn develops quickly after antigen exposure because of preformed antibodies

62
Q

which hypersensitivities have antibody-mediated components

A

types 1,2, and 3 (not 4!)

63
Q

Run through Type 2 hypersensitivity rxn

A

Cytotoxic
antibody mediated

Humoral:
IgG and IgM autoantibodies
Complement activation

Cellular:
NK cells
Eosinophils
Neutrophils
Macrophages

Coombs testing comes into play

examples incl acute hemolytic transfusion rxns
autoimmune hemolytic anemia
Goodpasture syndrome

IgM and IgG bind to fixed antigen on an “enemy” cell and cause cellular destruction.

IgM is most classic in activating Complement cascade

64
Q

Run through Type 3 hypersensitivity rxn

A

Immune complex:
antigen-antibody complex activates complement, which attracts neutrophils
neutrophils release lysosomal enzymes

this is usually IgG

in type 3 reaction, imagine 3 things stuck together:
Antigen-Antibody-Complement

Examples:
SLE nephritis
PSGN
Serum sickness

65
Q

Run through Type 4 hypersensitivity rxn

A

delayed type

No humoral component (no antibodies)

cellular component:
T cells!!!
Macrophages

T cells encounter antigen, release cytokines, and activate macrophages

Examples:
4 T's:
T cells
Transplant rejection!!
TB skin test!!
Touching (contact dermatitis)
66
Q

what type of hypersensitivity rxn creates a blood transfusion rxn

A

Type 2- preformed antibodies agains the foreign blood antigens

67
Q

what type of anemias do thalassemia cause

A

microcytic

68
Q

what is the strongest predisposing risk factor for pyelonephritis

A

vesicoureteral reflux

69
Q

what is the urinary incontinence associated with T1DM

A

overflow incontinence

70
Q

what is overflow incontinence

A

incomplete emptying,
causing leak with overfilling
you also have high post-void residual volume

this is due to detrusor UNDERactivity (impaired contractility) or an outlet obstruction (tumor)

71
Q

what is stress incontinence

A

urethral hyper mobility or intrinsic sphincter deficiency

leak with increased abdominal pressure

72
Q

what is urge incontinence

A 
overactive bladder (detrusor instability),
which causes leak with urge to void immediately

you have uninhibited bladder contraction

73
Q

what nerves have the micturition reflex

A

S2-S4

74
Q

what are the parasympathetic and sympathetic bladder actions

A

parasympathetic stimulation:
detrusor contract
internal urethral sphincter relax

sympathetic stimulation:
internal sphincter contract
help sense a full bladder

75
Q

what causes bladder problems in MS pts

A

uninhibited bladder contraction, an urge incontinence

76
Q

how do antimuscarinics work with urge incontinence

A

M3 receptor on the bladder:

stimulate: detrusor contraction
inhibit: detrusor relaxation –> urinary retention

77
Q

what does the TATA box do

A

promotor region that binds transcription factors and RNA polymerase II during initiation phase of transcription

78
Q

what is a way to dx/recognize central diabetes insipidus

A

polyuria that resolves with administration of desmopressin

because CDI is likely 2/2 a deficient vasopressin secretion

79
Q

what is vasopressin’s MOA

A

a V2 receptor-mediated increase in water permeability within the collecting ducts

as water leaves, urea concentration greatly increases

the collecting duct is impermeable to urea, but vasopressin activates urea transporters in the medullary collecting duct, increasing urea reabsorption and decreasing renal urea clearance. this allows for maximally concentrated urine

80
Q

how does EPI treat anaphylaxis

A

agonist at:

alpha-1:
vasoconstriction to increase BP

beta-1:
increase cardiac contractility and CO improves BP and peripheral perfusion

beta-2:
bronchodilation

81
Q

how do ventilation and perfusion vary across a lung

A

perfusion greatly increases from the apex to the base

ventilation increases slightly from the apex to the base

the V/Q ratio is highest at the apex, lowest at the base

82
Q

what is the cause of septic shock

A

release of endotoxins into the bloodstream

83
Q

what is gram-negative sepsis caused by

A

caused by the release of LPS from bacterial cells during division or bacteriolysis

LPS is not actively secreted by bacteria!!!
Lipid A is the toxic component of LPS
it causes activation of macrophages,
leading to widespread release of IL-1 and TNF-alpha,
which cause the signs/symptoms of septic shock:

fever, hypotension, diarrhea, oliguria, vascular compromise, DIC

(LPS = lipopolysaccharide)

84
Q

what is responsible for Gram Negative sepsis

A

Lipid A

85
Q

what is anaplastic

A

poorly differentiated

86
Q

what are curling ulcers

A

stress ulcers arising in the setting of severe trauma/burns

hypovolemia and mucosal ischemia

“burned by the curling iron”

87
Q

what are cushing ulcers

A

brain injury,
causing increased vagal stimulation,
increased ACh,
increased H+ secretion

“always cushion the brain”

88
Q

what is abetalipoproteinemia

A

inherited inability to synthesize apolipoprotein B,
an important component of chylomicrons and VLDL

lipids absorbed by the small intestine cannot be transported into the blood,
and accumulate in the interstitial epithelium,
resulting in RBCs with clear or foamy cytoplasm

89
Q

what is Whipple disease

A 
infection with T Whipplei.
PAS (+)
foamy macrophages in interstitial lamina propria
mesenteric nodes
Cardiac symptoms
Arthralgia's
Neurologic symptoms

“Foamy whipped cream in a CAN”

90
Q

what activates aldosterone release

A

Angiotensin 2 and extracellular K

91
Q

what activates glucocorticoid release

A

ACTH

92
Q

what activates catecholamine release

A

acetylcholine acts on medullary chromaffin cells

93
Q

what si the pathogenesis of pulmonary arterial hypertension (idiopathic/hereditary)

A

often due to inactivating mutation in BMPR2

predisposition for endothelial and SM cell proliferation.

vasoconstriction
vascular SM proliferation
intimal thickening and fibrosis
increased pulmonary vascular resistance
progressive pulmonary HTN
94
Q

where is the most common site of unilateral fetal hydronephrosis

A

inadequate canalization of the ureteropelvic junction (kidney and ureter connection)

95
Q

what muscle are important for sitting up

A 
external abdominal oblique
rectus abdominus
hip flexors, including:
psoas major
psoas minor
iliacus
96
Q

what do you see in liver injury 2/2 inhaled anesthetic hepatotoxicity

A

elevated serum LFTs and prolonged PTT
leukocytosis
eosinophilia

may give you a h/o recent surgery in another country (that uses halothane)

97
Q

what type are the blood type antibodies

A

A and B are IgM

type O mothers have predominately IgG antibodies, which can cross the placenta and cause fetal hemolysis

98
Q

what is the buzzword for eggwhites

A

biotin

99
Q

what does biotin do

A

cofactor for carboxylation enzymes (add 1-C)

pyruvate carboxylase:
pyruvate –> oxaloacetate
(gluconeogenesis)

acetyl-CoA carboxylase
acetyl-CoA –> malonyl-CoA
(Fatty acid synthesis)

propionyl-CoA carboxylase
propionyl-CoA –> methylmalonyl-CoA
(Fatty acid oxidation)

100
Q

what forms granulomas in TB

A

longhand cells have multiple nuclei peripherally organized in a horseshoe shape.
the macrophages that form these giant cells are activated by CD4+ Th1 cells

101
Q

what is the buzzword for mitochondrial myopathy

A

“ragged red fibers”!!!

blotchy red muscle fibers on Gomori trichrome stain

102
Q

what are mitochondrial myopathies

A

failure in oxidative phosphorylation, often present with lactic acidosis and myopathy, and CNS disease

103
Q

what is the CF mutation

A

CFTR 3-base pair deletion at deltaF508.

this mutation impairs post-translational processing (folding) of CFTR, resulting in shunting of CFTR toward the proteasome, with complete absence of the protein on the cell surface

104
Q

what is polygenic inheritance

A

depends on several genetic factors with its inheritance

a key example is androgenic alopecia,
which factors in genes on X and Y chromosomes

105
Q

what do chronic glucocorticoids do to the HPA axis

A

it decreases CRH, ACTH, and cortisol levels

they cannot rise in response to a stress

the exogenous glucocorticoids has a negative feedback on the ENTIRE HPA axis

106
Q

what is nephrotic syndrome associated with

A

a hypercoagulable state

you lose anticoagulant factors, especially antithrombin III, is responsible for thrombotic and thromboembolic complications of nephrotic syndrome

107
Q

what heart sounds do you hear with constrictive pericarditis

A

Kussmaul sign (increase in JVP on inspiration, vs decrease in a normal heart)

pulsus paradoxus

may also be pericardial knock (even earlier than S3)

108
Q

when do you hear a lout P2

A

pulmonary HTN

109
Q

when do you hear mid-systolic click

A

mitral valve prolapse

110
Q

when do you hear S3

A

restrictive cardiomyopathy- reduced intrinsic ventricular wall compliance

common in dilated ventricles

111
Q

when do you hear S4

A

atrial kick late in diastole
high atrial pressure

associated with ventricular noncompliance- push against a stiff wall

Daily Flashcard Quizzes (21 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions