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
2
Q
what are standard precautions for C diff
A
wash with soap and water
gown
non sterile gloves
(masks are for droplet precautions)
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”
4
Q
what is Berkson’s bias
A
selection bias when you’re selecting hospitalized (sick) pts as your control group
5
Q
what are asplenic pts at risk for
A
infection with encapsulated bacteria SHiN Strep pneumo Haemophilus Influenzae Neisseria
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”
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”
8
Q
where is complement produced
A
liver
9
Q
what is immediate hypersensitivity
A
results from IgE-mediated mast cell degranulation
“imEEEdiate”
10
Q
what is the only fungus that has a polysaccharide capsule
A
cryptococcus neoformans
11
Q
what organism pairs with the ‘Micicarmine stain” buzzword
A
cryptococcus neoformans
it appears red on this stain
12
Q
what is reaction formation
A
taking negative thoughts/feelings and doing the exact opposite
13
Q
what is splitting
A
see something as “all good” or “all bad”
often with a borderline personality disorder
14
Q
what is somatic symptom disorder
A
extreme preoccupation with unexplained medical symptoms and excessive health care use
symptoms are not intentional
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
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
17
Q
what is a t-test for
A
compare difference between the means of 2 groups
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”
19
Q
what is a Chi square test for
A
used to evaluate the association between 2 categorical variables
ALL qualitative variables
“chi-tegorical”
20
Q
what are anti-Smith antibodies specific for
A
SLE
21
Q
what are anti-Smith antibodies’ target
A
autoantibodies against snRNPs
22
Q
what can a SLE pt with anti-Smith antibodies not do
A
remove introns from RNA transcripts
23
Q
what is wet and dry beriberi
A
2/2 thiamine deficiency
dry:
bilateral peripheral neuropathy
wet:
neuropathy + CHF
24
Q
what is B6 deficiency characterized by
A
cheilosis, glossitis, dermatitis, affective symptoms (irritability)
sideroblastic anemias
25
what does Thiamine used for
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)
26
how does colchicine help in gout
binds and stabilizes tubulin to inhibit microtubule polymerization, which will impair NEUTROPHIL chemotaxis and degranulation
acute and prophylactic value
27
what is the bruising process
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
28
what suggests a general nephritic syndrome
HTN, hematuria, and moderate proteinuria
29
what are linear deposits made of on renal biopsy, and what are they characteristic of
mad elf IgG and C3
anti-glomerular BM disease
30
what are the different immunofluorescent findings in RPGN
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
31
what is the characteristic renal pathology in a lupus pt? 2nd most likely?
Diffuse proliferative glomerulonephritis!!!
or if it's nephrotic,
Membranous Glomerulonephritis
32
how do you differentiate between Goodpasture and Wegener
Goodpasture:
lung
kidney
linear IF (anti-GBM)
```
Wegener:
"C disease"
Nasopharynx!!!
lung
kidney
c-ANCA (negative IF)
```
33
how do you differentiate between Churg-Strauss and Microscopic Polyangiitis
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
34
what do you see on membranoproliferazive glomerulonephritis
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
35
which 2 renal diseases have effacement of podocyte foot processes
minimal change disease
focal segmental glomerulonephritis
36
which 2 renal pathologies have immune complex deposition giving a granular IF
membranous nephropathy
membranoproliferazive glomerulonephritis
37
which 2 renal pathologies are 2/2 systemic disease that affect glomeruli
Diabetes
systemic amyloidosis
38
what are Kimmelstiel-Wilson nodules a buzzword for
diabetic nephropathy
they're nodules of sclerosis within the glomeruli
39
which cancer is Minimal change disease associated with
Hodgkin Lymphoma
Reid Sternberg cells produce massive cytokines
40
which renal pathology gives you spike and dome appearance on EM
membranous nephropathy
thick membranes + immune complex deposition
41
what diseases are membranous nephropathy associated with
Hepatitis B,C
SLE if it's not Diffuse proliferative glomerulonephritis
42
how do you identify systemic sclerosis affecting kidneys
apple-green birefringence with Congo Red staining 2/2 amyloid deposits!!
43
what stain apple-green with congo-red stain
Amyloidosis!
44
what is Berger disease
AKA IgA nephropathy!
IgA immune complex deposition in mesangium
commonly in childhood
with RBC casts
following mucosal infection
45
what can IgA nephropathy be associated with
Henoch Schonlein Purpura!!!
with palpable purpora on buttocks, arthralgia, GI pain 2/2 URI commonly
both have IgA deposition
46
what is Alport syndrome
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
what is the AR equation and the ARR equation, and which NNT/NNH does each pair with
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
what is NNH equation and the NNT equation
NNH = 1 / AR
NNT = 1/ARR
49
how can you accelerate fetal lung development in a pregnant mom expecting a preterm baby
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
what is the rapid treatment option for RA relief
NSAIDs and glucocorticoids help provide immediate, short-term relief
51
what can a pt with anti-phospholipid antibodies have
pt has SLE
52
what do anti-phospholipid antibodies do
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
how long does it take to lose cardiomyocyte contractility after onset of total ischemia
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
what is Hyper-IgM syndrome
```
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
what immunoglobulins are on naive B cells
IgM and IgD prior to activation
this is why a hyper-IgM pt with defect in CD40L can still produce an IgM response
56
distinguish transference and displacement
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
distinguish Type 1 from Type 2 muscle fibers
```
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
why are skeletal muscles not affected by CCBs
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
which lymphocytes are seen in the peripheral blood smears of pts with EBV
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
what are the 4 types of hypersensitivity reactions
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
Run through Type 1 hypersensitivity rxn
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
which hypersensitivities have antibody-mediated components
types 1,2, and 3 (not 4!)
63
Run through Type 2 hypersensitivity rxn
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
Run through Type 3 hypersensitivity rxn
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
Run through Type 4 hypersensitivity rxn
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
what type of hypersensitivity rxn creates a blood transfusion rxn
Type 2- preformed antibodies agains the foreign blood antigens
67
what type of anemias do thalassemia cause
microcytic
68
what is the strongest predisposing risk factor for pyelonephritis
vesicoureteral reflux
69
what is the urinary incontinence associated with T1DM
overflow incontinence
70
what is overflow incontinence
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
what is stress incontinence
urethral hyper mobility or intrinsic sphincter deficiency
leak with increased abdominal pressure
72
what is urge incontinence
```
overactive bladder (detrusor instability),
which causes leak with urge to void immediately
```
you have uninhibited bladder contraction
73
what nerves have the micturition reflex
S2-S4
74
what are the parasympathetic and sympathetic bladder actions
parasympathetic stimulation:
detrusor contract
internal urethral sphincter relax
sympathetic stimulation:
internal sphincter contract
help sense a full bladder
75
what causes bladder problems in MS pts
uninhibited bladder contraction, an urge incontinence
76
how do antimuscarinics work with urge incontinence
M3 receptor on the bladder:
stimulate: detrusor contraction
inhibit: detrusor relaxation --> urinary retention
77
what does the TATA box do
promotor region that binds transcription factors and RNA polymerase II during initiation phase of transcription
78
what is a way to dx/recognize central diabetes insipidus
polyuria that resolves with administration of desmopressin
because CDI is likely 2/2 a deficient vasopressin secretion
79
what is vasopressin's MOA
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
how does EPI treat anaphylaxis
agonist at:
alpha-1:
vasoconstriction to increase BP
beta-1:
increase cardiac contractility and CO improves BP and peripheral perfusion
beta-2:
bronchodilation
81
how do ventilation and perfusion vary across a lung
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
what is the cause of septic shock
release of endotoxins into the bloodstream
83
what is gram-negative sepsis caused by
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
what is responsible for Gram Negative sepsis
Lipid A
85
what is anaplastic
poorly differentiated
86
what are curling ulcers
stress ulcers arising in the setting of severe trauma/burns
hypovolemia and mucosal ischemia
"burned by the curling iron"
87
what are cushing ulcers
brain injury,
causing increased vagal stimulation,
increased ACh,
increased H+ secretion
"always cushion the brain"
88
what is abetalipoproteinemia
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
what is Whipple disease
```
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
what activates aldosterone release
Angiotensin 2 and extracellular K
91
what activates glucocorticoid release
ACTH
92
what activates catecholamine release
acetylcholine acts on medullary chromaffin cells
93
what si the pathogenesis of pulmonary arterial hypertension (idiopathic/hereditary)
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
where is the most common site of unilateral fetal hydronephrosis
inadequate canalization of the ureteropelvic junction (kidney and ureter connection)
95
what muscle are important for sitting up
```
external abdominal oblique
rectus abdominus
hip flexors, including:
psoas major
psoas minor
iliacus
```
96
what do you see in liver injury 2/2 inhaled anesthetic hepatotoxicity
elevated serum LFTs and prolonged PTT
leukocytosis
eosinophilia
may give you a h/o recent surgery in another country (that uses halothane)
97
what type are the blood type antibodies
A and B are IgM
type O mothers have predominately IgG antibodies, which can cross the placenta and cause fetal hemolysis
98
what is the buzzword for eggwhites
biotin
99
what does biotin do
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
what forms granulomas in TB
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
what is the buzzword for mitochondrial myopathy
"ragged red fibers"!!!
| blotchy red muscle fibers on Gomori trichrome stain
102
what are mitochondrial myopathies
failure in oxidative phosphorylation, often present with lactic acidosis and myopathy, and CNS disease
103
what is the CF mutation
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
what is polygenic inheritance
depends on several genetic factors with its inheritance
a key example is androgenic alopecia,
which factors in genes on X and Y chromosomes
105
what do chronic glucocorticoids do to the HPA axis
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
what is nephrotic syndrome associated with
a hypercoagulable state
you lose anticoagulant factors, especially antithrombin III, is responsible for thrombotic and thromboembolic complications of nephrotic syndrome
107
what heart sounds do you hear with constrictive pericarditis
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
when do you hear a lout P2
pulmonary HTN
109
when do you hear mid-systolic click
mitral valve prolapse
110
when do you hear S3
restrictive cardiomyopathy- reduced intrinsic ventricular wall compliance
common in dilated ventricles
111
when do you hear S4
atrial kick late in diastole
high atrial pressure
associated with ventricular noncompliance- push against a stiff wall
