Some CV and renal conditions and DM drugs Flashcards

1
Q

S3

A

Early diastole
Associated with INCREASED FILLING PRESSURES (MR, HF); More common in dilated ventricles
Normal in children, pregnant women

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2
Q

S4

A

Late diastole - ‘Atrial kick’ due to high atrial pressure
Associated with ventricular hypertrophy and stiff LV wall
Best heard in left lateral decubitus

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3
Q

Normal S2 splitting

A

A2-P2 widens slightly with inspiration
Inspiration -> drop in intrathoracic pressure -> increased venous return -> increased RV filling and SV -> INCREASED RV EJECTION TIME-> Delayed closure of PV in cycle compared to AV

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4
Q

Wide S2 splitting

A

A2-P2 exaggeratedly split

CONDITIONS THAT DELAY RV EMPTYING (PS, RBBB) -> Delayed PV closure regardless of breath, but increases with inspiration

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5
Q

Fixed S2 splitting

A

A2-P2 exaggeratedly split and unchanging
OCCURS IN ASD
L->R shunt increases RA/RV volumes -> Delayed PV closure regardless of breath that DOESN’T CHANGE WITH INSPIRATION

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6
Q

Paradoxical S2 splitting

A

Conditions that delay AV closure (AS, LBBB) -> Reversal of normal valve closure order -> P2-A2 heard
On inspiration -> Increased RV ejection time -> P2 heard later and closer to A2 -> Split narrows instead of widening

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7
Q

Kussmaul sign

A

Increased JVP on inspiration instead of normal decrease

Due to impaired RV filling with constrictive pericarditis, restrictive cardiomyopathies, tumors in RA/RV

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8
Q

PAN

A

Medium vessel vasculitis in young adults affecting renal, visceral vascular beds, but NOT PULM aa
Sx based on affected organs
Due to immune complexes -> Fibrinoid necrosis
Associated w/ HBV

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9
Q

micro-PAN

A

Necrotizing vasculitis commonly involving lung, kidneys, and skin w/ pauci-immune glomerulonephritis and palpable purpura
Presents as granulomatosis with polyangiitis without nasopharyngeal involvement
No granulomas, asthma, or eosinophilia (vs. Churg-Strauss)

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10
Q

Nephritic syndromes

A

Inflammatory conditions -> Hematuria, RBC casts in urine; Azotemia, oliguria, HTN, mild proteinuria
Acute PSGN, RPGN (crescentic), DPGN, IgA nephropathy (Berger disease), Alport syndrome, MPGN

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11
Q

Nephrotic syndromes

A

Podocyte damage disrupting glomerular filtration charge barrier -> Massive proteinuria, hypoalbuminemia, hypogammaglobulinemia, edema, hyperlipidemia
Frothy urine with fatty casts
Hypercoagulable state due to ATIII loss
Minimal change disease, FSGS - No IC deposits, podocyte foot process effacement only
Membranous nephropathy, MPGN - Granular IF
Amyloidosis, DM glomerulonephropathy - due to systemic conditions

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12
Q

Acute PSGN

A

Nephritic
Enlarged, hypercellular glomerulid
Granular IF w/ IgG, IgM, C3 deposition in GBM and mesangium
Subepithelial IC humps, low serum C3

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13
Q

RP (crescentic) GN

A

Nephritic
Crescent-shaped deposits of fibrin, plasma protein (e.g. C3b), and macrophages
Poor prognosis
Associated w/ Goodpasture syndrome, Wegener’s granulomatosis w/ polyangiitis, and microscopic polyangiitis

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14
Q

DPGN

A

Mixed nephritic/nephrotic
SLE nephritis - most common COD
Subendothelial or intramembranous IgG ICs w/ C3 deposition - granular IF

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15
Q

IgA nephropathy

A

Nephritic
AKA Berger disease
IgA IC deposits in mesangium -> mesangial proliferation
Episodic hematuria w/ RBC casts presenting after acute gastroenteritis
Renal pathology of Henoch-Schonlein purpura

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16
Q

Alport syndrome

A

Nephritic
XR mutation of type IV collagen -> GBM splitting
Retinopathy, lens dislocation, glomerulonephritis, sensorineural deafness

17
Q

MPGN

A

Mixed nephritic/nephrotic
T1 - Subendothelial granular ICs w/ ‘tram-track’ appearance due to GBM splitting caused by mesangial ingrowth. Associated w/ HBV, HCV
T2 - Intramembranous dense IC deposits. Associated w/ C3 nephritic factor -> stabilized C3 convertase -> low serum C3

18
Q

FSGS

A

Nephrotic
Segmental sclerosis/hyalinosis of glomeruli
Nonspecific IF w/ podocyte foot process effacement
Most common nephrotic syndrome in African Americans, Hispanics. Associated w/ HIV, heroin, sickle cell

19
Q

Minimal change disease

A

Nephrotic
Normal glomeruli w/ negative IF, podocyte foot process effacement
Most common in children, often triggered by recent immune stimulus or rarely 2o to lymphoma
Cytokine mediated -> Only nephrotic syndrome w/ good response to corticosteroids

20
Q

Membranous nephropathy

A

Nephrotic
Diffuse capillary and GBM thickening
Granular IF w/ ‘spike and dome’ subepithelial IC deposits
SLE nephrosis
Most common in white adults. Associated w/ SLE, HCV, HBV
(MPGN has similar IF deposition and proteinuria)

21
Q

Amyloidosis

A

Nephrotic
Mesangial amyloid deposits
Associated w/ chronic immune/inflam conditions - multiple myeloma (cast nephropathy w/ Bence-Jones proteins), TB, RA
Kidney is most commonly involved organ of systemic amyloidosis

22
Q

DM glomerulonephropathy

A

Nephrotic
Eosinophilic nodular glomerulosclerosis (Kimmelstiel-Wilson nodules) w/ mesangial expansion, GBM thickening
Due to non-enzymatic glycosylation of GBM (poor charge barrier -> nephrosis) and efferent arterioles (up GFR; give ACE inhibitors/ARBs to DM patients)

23
Q

Metformin

A

Down gluconeogenesis, up glycolysis, up insulin sensitivity
Most serious SE is lactic acidosis -> CI in HF, renal insufficiency
Can be used in T1DM - islet fxn not required

24
Q

Sulfonylurea 1st gen

A

Chlorpropamide, Tolbutamide
Stimulate release of endogenous insulin in T2DM
Risk of hypoglycemia in renal failure from low drug excretion
1st gen SE: Disulfiram-like rxn

25
Q

Sulfonylurea 2nd gen

A

Glimepiride, Glipizide, Glyburide
Stimulate release of endogenous insulin in T2DM
Risk of hypoglycemia in renal failure from low drug excretion
2nd gen SE: Hypoglycemia

26
Q

Glitazones/TzDs

A

Pioglitazone, Rosiglitazone
Bind PPAR-g in periphery to up insulin sensitivity in T2DM
SE: Weight gain, edema, HF, osteoporosis
No hepatotoxicity associated w/ current TzDs (but previous versions had this risk)

27
Q

GLP-1 analogs

A

Exenatide, Liraglutide
Trigger glucose-dependent insulin release in T2DM
SE: Nausea, vomiting, pancreatitis

28
Q

DPP-4 inhibitors

A

Linagliptin, Saxagliptin, Sitagliptin
Block GLP-1 degradation in T2DM
SE: Mild urinary/resp infections

29
Q

Amylin analogs

A

Pramlintide
Delays gastric emptying, suppresses glucagon in BOTH types of DM
SE: Hypoglycemia, nausea, diarrhea

30
Q

SGLT-2 inhibitors

A

Canagliflozin
Block reabsorption of glucose in PCT in T2DM
SE: Glucosuria causing UTIs, yeast infections

31
Q

a-glucosidase inhibitors

A

Acarbose, Miglitol
Block intestinal brush-border a-glucosides to limit glucose absorption -> decreased postprandial hypoglycemia in T2DM
SE: Nausea, vomiting, flatulence