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Spring 2016 - CVPR > Renal > Flashcards

Renal Flashcards

1
Q

What is the main physiological function of the kidneys?

A

Maintenance of the composition and volume of extracellular fluid

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2
Q

What is extracellular fluid?

A

Fluid outside cells, but on the serosal side of epithelial tissues

So, bladder urine, GI tract fluid, and lung fluid are not ECF

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3
Q

How much extracelular fluid do we have? What are the 2 main compartments?

A

15 L

12L interstitial fluid
3 L Plasma

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4
Q

How do we maintain homeostasis of stuff in the extracellular fluid?

A

Through urine production

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5
Q

What are the 2 capillary beds of the kidneys?

A

Glomerular

Peritubular

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6
Q

What is glomerular filtration?

A

Filtration of plasma into the tubule.

Allows water and solutes in, but retains larger colloids

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7
Q

What is the filtration fraction? What is its normal value?

A

Amount of renal plasma flow filtered at the glomerulus.

20% of renal blood flow

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8
Q

What induces the kidneys to secrete renin? (3)

A

Activation of renal beta-sympathetic nerves

Stimulation of renal baroreceptors by decreased arteriolar pressure

Activation of macula densa chemoreceptor by reduced delivery of NaCl to the distal rubule

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9
Q

Which cells in the kidney secrete renin? Where are they? What structure are they part of?

A

Granular cells, in the afferent arteriole going to the glomerulus

Juxtaglomerular apparatus

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10
Q

The molecular sieving process of the glomerulus is also called _______________

A

Ultrafiltration

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11
Q

What is filterability a function of?

A

Molecular size

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12
Q

What are the 3 filters of the glomerulus?

A

Fenestrated epithelium

Basal lamina

Podocytes

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13
Q

What is the charge of the basal lamina?

A

Negative, so negatively charged things don’t get through

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14
Q

Mathematical description for GFR

A

GFR = dP/R = KdP = K(Pgc-Pt-Pigc)

Pressures of glomerular capillary, tubule, colloid osmotic pressure)

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15
Q

What are 2 forces that oppose glomerular filtration?

A

Tubule diameter -> backpressure = Pt

Colloid osmotic force

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16
Q

What is the net filtration pressure?

A

Sum of glomerular capillary, tubule, colloid osmotic pressures

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17
Q

What do mesangial cells do? (3)

A

Secrete matrix continuous with basal lamina

Do some macrophage-like things (make cytokines, etc)

Unclear role in contraction of glomerular capillary loops

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18
Q

Is glomerular capillary pressure dependent on mean arterial pressure?

A

No. It is very tightly autoregulated

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19
Q

What is the glomerular response to chronic hypotension?

A

Both the afferent and efferent arterioles constrict

This decreases flow through the glomerulus (so it can go to other organs) but sort of maintains Pgc (glomerular capillary pressure)

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20
Q

3 baroreceptors that affect glomerular arterioles

A

Baroreceptors in main arteries -> sympathetic response

External baroreceptors -> antiogensin II constricts

Intrarenal baroreceptors -> RAAS

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21
Q

Where are renal interstitial cells located? What do they do?

A

Located in kidney medulla between renal pyramids

Make renal prostaglandins

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22
Q

When are renal prostaglandins produced? What do they do?

A

Secreted in response to angiotensin II

Dilate renal arterioles -> maintain adequate renal blood flow, maintain GFR. This blunts effects of hypovolemic mechanisms so the kidney doesn’t get ischemic

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23
Q

Compare autoregulation and hypovolemic response:

Responds to
Purpose
Arterioles involved
Mechanism of arteriolar changes
Location of mechanism
A

mrr

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24
Q

What do the minor calyxes do? Major calyx?

A

Drain renal pyramids

Drain minor calyxes

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25
Q

What do the medullary pyramids contain?

A

Nephrons and collecting ducts

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26
Q

What is the path of the renal arteries to veins?

A

Renal artery -> anterior and posterior segments -> interlobar (between medullary pyramids) -> arcuate arteries (parallel to outer capsule) -> interlobular -> afferent arterioles -> glomerular capillary -> efferent arterioles -> vasa recta ? -> peritubular capillary -> interlobular veins -> arcuate veins -> interlobar veins -> renal vein

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27
Q

What part of the kidney are renal corpuscles located in?

A

Cortex

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28
Q

What part of the kidney are renal tubules in?

A

Medulla

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29
Q

What kind of epithelium is in the proximal tubule?

A

Cuboidal with brush border

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30
Q

What does the proximal tubule transport?

A

Na/K ATPase for pumping sodium out of the basolateral side

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31
Q

What is the epithelium like in the thin loop of Henle?

A

Simple squamous

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32
Q

What is the epithelium like in the thick loop of Henle?

A

Cuboidal

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33
Q

What is the epithelium like in the distal tubule?

A

Cuboidal

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34
Q

Where do aldosterone and antidiuretic hormone act in the kidney?

A

Distal tubule

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35
Q

What two hormones act on the distal tubule?

A

Aldosterone

Antidiuretic hormone

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36
Q

The distal convoluted tubule is physically connected to the region near the vascular pole through the _______

A

Macula densa

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37
Q

Where are the Lacis cells located?

A

Between macula densa and mesangial cells

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38
Q

What is another name for antidiuretic hormone?

A

Vasopressin

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39
Q

What is the major osmotic substance in the ECF?

A

Sodium

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40
Q

Where are the osmoreceptors?

A

Supraoptic nucleus of the hypothalamus

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41
Q

What makes antidiuretic hormone?

A

Hypothalamus (specifically, the supraoptic nucleus)

OR maybe the pituitary

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42
Q

Mental states with increased risk of suicide

A

Hopelessness
Helplessness
Impulsivity

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43
Q

Are all patients who kill themselves depressed?

A

No

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44
Q

How do you protect against suicide in schizophrenia?

A

Clozapine

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45
Q

What CSF substance is associated with an increased risk of violence and suicide?

A

5-HIAA (hydroxyindoleacetic acid)

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46
Q

What are 2 groups of people who are at high risk of completing suicide?

A

Single male who lives alone

Chronic physical illness

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47
Q

7 psychiatric illnesses that predispose to suicide

A 
Depression
Schizophrenia
Bipolar mood disorder
Drug or alcohol problems
Cognitive disorder
Anorexia nervosa
Personality disorder with axis I co-morbidity
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48
Q

When is risk of suicide highest in renal disease? What does this mean?

A

First 3 months of dialysis

Suicide is prompted by failure to cope with stress rather than declining health status

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49
Q

5 errors made in the evalulation of psychiatric patients

A

Not corroborating story with family/friends
Not reviewing old records
Not seeking consultation
Avoiding specific questions about guns, plans, fantasies, etc
Ignoring risk enhancing factors

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50
Q

How much fluid is in the intracellular compartment? What are the 2 parts?

A

27L
Noncirciulating cell volume = 24L
Blood cells = 3L

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51
Q

What are the insensible water losses?

A

Respiration, skin

The ones you can’t sense I guess

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52
Q

How much of the cardiac output do kidneys recieve?

A

25%

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53
Q

Why do filtration and reabsorption rates&raquo_space; excetion rates?

A

Rapid removal of waste products

Precise and rapid volume/composition control of ECF

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54
Q

What important calcium-related substance does the renal system make?

A

Calcitriol

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55
Q

What is the rate-limiting step of the RAAS?

A

Renin

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56
Q

What happens to net filtration pressure as we move along the tubule?

A

It decreases and eventually reaches equilibrium

This is because Pi gc increases and Pgc-Pt decreases

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57
Q

What 2 things make up K, the resistance term in GFR = dP*K?

A

Hydraulic conductivity
Surface area

K = pA

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58
Q

What 2 things determine filtration fraction?

A

FF = GFR/RPF

RPF = renal plasma fraction

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59
Q

Which arteriole does angiotensin II act on?

A

Both, but mostly the efferent (away) one

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60
Q

How do NSAIDS affect the kidneys?

A

They block prostaglandins, vasoconstricting the afferent arteriole

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61
Q

How do ACEIs and ARBs affect the kidneys?

A

They block angiotensin II, increasing renal blood flow but decreasing GFR

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62
Q

What is the pH of the urine of carnivores and herbivoes?

A

Carnivores - acidic

Herbivore - alkaline

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63
Q

What are the 2 sides of the epithelial cells in the renal tubules?

A

Apical - faces lumen

Basolateral - faces serosa (interstitium and capillaries)

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64
Q

What side are microvilli on?

A

Apical

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65
Q

How many ions/molecules does a facilitated diffusion carrier take?

A

At least 2 (why not 1?)

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66
Q

What side is the Na/K ATPase on? Which directions does it transport?

A

Basolateral

3 Na out, 2K in

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67
Q

What are the jobs of the nephron segments?

A

Proximal convoluted tubule - bulk reabsorption
Loop of Henle - urine dilution
Distal convoluted tubule - tine-tuning Na balance
Collecting duct - fine-tuning K, acid, water ballance

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68
Q

10 things the proximal tubule cell does

A

Bulk reabsorption of: Na, water, glucose, amino acids, calcium, phosphate, citrate
H+ secretion/HCO3 absorption
Organic anions secretion
Macromolecule absorption

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69
Q

Is the thick ascending limb permeable to water?

A

No

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70
Q

What 3 things are reabsorbed in the thick ascending limb?

A

Na (trans-Na/K/2Cl cotransporter and paracellular)
Ca (paracellular)
Mg (paracellular)

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71
Q

What 3 things are reabsorbed in the distal convoluted tubule?

A

Na (Na/Cl cotransporter)
Ca
Mg

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72
Q

Where do thiazide diuretics act?

A

Distal convoluted tubule NaCl cotransporter

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73
Q

2 types of cells in the collecting duct

A 
Principal cells
Intercalated cells (alpha, beta)
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74
Q

What do principal cells do (3)?

A

Fine tune Na (ENaC), K (ROMK/Maxi), water (aquaporin) reabsorption in the collecting duct

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75
Q

What do alpha intercalated cells do?

A

H+ secretion
HCO3- synthesis
K+ absorption

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76
Q

What do beta intercalated cells do?

A

HCO3- secretion

CL- absorption

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77
Q

What does aldosterone do to the principal cells in the collecting duct?

A

Increases Na+ transporters so Na+ goes into the blood

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78
Q

What does vasopressin do the collecting duct?

A

Allows it to be permeable to water via aquaporins

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79
Q

How does tubular function depend on flow?

A

Higher velocity - less time for interaction with transporters -> less absorption

Reduced flow rate increases absorption

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80
Q

How do receptors for ECF volume work?

A

Stretch

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81
Q

4 effects ofsympathetic activity on the kidney

A

Vasoconstriction
Renin release
Decreased RBF/GFR
Increased renal reabsorption of NaCl

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82
Q

Where is aldosterone made?

A

Adrenal gland

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83
Q

What does vasopressin do?

A

Induces expression of aquaporins on collecting duct cells so water can escape out of the urine

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84
Q

8 non-osmotic stimuli for vasopressin

A 
Low effective arterial blood volume
Endocrine disorder
Pain
Nausea
CNS disorders
Pulmonary disorders
Drugs
Meds
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85
Q

What are the normal values for PO2
PCO2
and HCO3

A

94 +-8
38 +-2
24 +-2

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86
Q

What defines acute kidney injury?

A

Rapid reduction in glomerular filtration rate manifested by a rise in plasma creatinine and urea concentration

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87
Q

What state does acute kidney injury result in?

A

Reduced clearance of nitrogenous waste products

-> azotemia

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88
Q

What are 3 problems that can cause acute kidney injury?

A

Pre-renal azotemia - decreased GFR from decreased renal plasma flow or renal perfusion pressure

Post-renal azotemia or obstructive nephropathy - decreased GFR due to obstruction of urine flow

Intrinsic renal disease - decreased GFR from direct injury to the kidneys

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89
Q

What is oliguria?

What is anuria?

A

Decreased urine (

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90
Q

What is the most common cause of an abrupt decrease in GFR in a hospitalized patient?

A

Prerenal azotemia

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91
Q

What are 2 hypervolemic states that can cause pre-renal azotemia?

A

Congestive heart failure
Cirrhosis

These diseases are characterzed by low effective arterial blood volume and reduced renal perfusion

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92
Q

4 types of kidney diseases that cause acute kidney injury

A

Vascular (cholesterol emboli, renal vein thrombosis)
Glomerular (acute glomerulonephritis, hemolytic uremic syndrome)
Interstitial (acute interstitial nephritis, infection, myeloma kidney)
Tubular (ischemic or nephrotoxic acute tubular necrosis)

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93
Q

Where in the nephron do urinary casts usually form

A

Distal convoluted tubule

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94
Q

2 common causes of death in patients with acute tubular necrosis

A

Infections

GI bleed

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95
Q

What is the primary protein in the slit diaphragm of pedicels?

A

Nephrin

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96
Q

Why should we care about microalbuminuria?

A

Suggestive of early glomerular damage

We look for it in diabetics to predict diabetic nephropathy

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97
Q

What is nephrotic syndrome?

What is nephritic symdrome?

A

Nephrotic - protein leak through glomerular capillary wall

Nephritic - glomerular injury

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98
Q

5 things altered in nephrotic syndrome

A 
Protineuria
Hypoalbuminemia
Edema
Hyperlipidemia
Lipiduria
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99
Q

What are the 2 mechanisms by which edema occurs in nephrotic syndrome?

A

Decreased serum albumin

Defect in sodium excretion -> volume expansion

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100
Q

Why is there hyperlipidemia and increased risk for thrombosis in nephrotic syndrome?

A

The liver tries to make more albumen and it also makes more of all proteins, including lipoproteins and clotting factors

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101
Q

6 things altered in nephritic syndrome

A 
Microhematuria (sometimes casts)
Leukocyturia
Proteinuria
Decreased GFR
Hypertension
Edema
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102
Q

3 genes most commonly mutated in hereditary glomerular disease

A

Nephrin
Podocin
WT-1

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103
Q

How do you treat hereditary glomerular disease?

A

ACEI
Renal transplantation eventually

Steroids don’t work

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104
Q

What is the mechanism of minimal change disease?

A

A circulating permeability factor acts directly on the podocyte, disrupting the permeability barier so proteinuria occurs

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105
Q

What molecule is expressed with minimal change disease?

A

CD80

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106
Q

What is the treatment for minimal change disease?

A

Steroids

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107
Q

What genetic polymorphism is more common in focal segmental glomerulosclerosis?

A

APOL1

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108
Q

What is membranous nephropathy?

A

Deposition of immune complexes in subepithelial space - glomerular basement membrane looks thickened

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109
Q

What is the antigen n membranous nephropathy?

A

Something on the podocyte, usually PLA2

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110
Q

What is the histologic pattern in membranoproliferative glomerulonephritis?

A

Mesangial proliferation
Thickening of glomerular basement membrane
C3 and IgG deposits

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111
Q

Membranoproliferative flomerulonephritis type 1 is associated with what infection?

A

Hepatitis C

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112
Q

What 2 diseases exhibit pulmonary-renal syndrome?

A

Goodpasture’s

ANCA-associated vasculitis

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113
Q

Crescents are ssociated with what disease process?

A

Rapidly progressing glomerulonephritis

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114
Q

Where are crescents? What 2 cells types are they made of?

A

Bowman’s capsule

Macrophages and parietal epithelial cells

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115
Q

Which infection is most common before post-infectious glomerulonephritis?

A

Group A strep (GAS)

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116
Q

In IgA nephropathy, wheredoes IgA usually deposit?

A

Mesangium

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117
Q

What is the mechanism of IgA nephropathy?

A

IgAs have abnormal sugars and are not cleared as easily, resulting in circulating complexes

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118
Q

What is the systemic disease that results in IgA nephropathy?

A

Henoch-Schonlein purpura

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119
Q

What is a pauci-immune renal vasculitis

A

Small vessel vasculities of the kidneys without evidence of immune complex deposition

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120
Q

What autoantibody is often present in pauci-immune renal vasculitis?

A

ANCA

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121
Q

What are the 2 most common antigens for ANCA?

A

Myeloperoxidase

PR-3

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122
Q

Cryoglobulins are most frequently associated with ________ infection

A

Hepatitis C

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123
Q

What do maltese crosses and oval fat bodies refer to?

A

The refractile pattern of lipiduria

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124
Q

3 complications of nephrotic syndrome

A

Hypercoagulability
Increased infections
Less vitamin D

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125
Q

3 things in general management of nephrotic syndrome

A

Low-salt diet
Diuretics
Blood pressure control

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126
Q

What is the main pathologic change in minimal change disease? What imaging modality is used to see it?

A

Elecron microscopy shows foot process fusion (but really foot processes are disrupted and proteinuria occurs)

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127
Q

What are 3 diseases associated with focal segmental glomerulosclerosis?

A

HIV associated nephropathy
Sickle cell
Obesity

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128
Q

What toxin can lead to membranous nephropathy?

A

Mercury

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129
Q

What is abnormal in membranoproliferative glomerulonephritis type II?

A

Low C3 and C4 via the alternative complement pathway

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130
Q

Are adjacent podocyte feet from the same cell or different cells?

A

Different! They alternate

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131
Q

5 clinical syndromes of glomerular disease

A

Asymptomatic hematuria/proteinuria

Acute nephritic syndrome (hematuria/protinuria + ARF)

Rapidly progressive nephritic syndrome

Nephrotic syndrome (massive proteinuria, hypoalbuminemia, edema)

Chronic renal failure

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132
Q

What are the 6 ‘nephritic’ diseases?

A

Benign familial hematuria (thin basement membrane disease)

Alport’s disease

IgA nephropathy

Postinfectious glomerulonephritis

Focal necrotizing/crescentif glomerulonephritis

Lupus glomerulonephritis

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133
Q

What is mutated in both thin basement membrane disease and Alport’s disease?

A

Collagen IV

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134
Q

What is the triad of Alport’s disease?

A

Nephritis
Deafness
Ocular lesions

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135
Q

What is the inheritance pattern of Alport’s disease

A

X-linked

I presume recessive

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136
Q

What population does Henoch-Schonlein Purpura most commonly occur in?

A
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137
Q

A starry sky immunoflourescence pattern occurs in which disease?

A

Postinfecious glomerulonephritis

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138
Q

What is the difference between membranous disease and membranoproliferative disease (both 1 and II)

A

Immune aggregates between the basement membrane and the podocyte

Immune aggregates in the basement membrane
I - antibodies
II - complement

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139
Q

3 types of IF staining in focal segmental necrotizing and crescentic glomerulonephritis

A

Linear - basement membrane itself is the antigen (Goodpasture’s, anti-GBM)

Granular - immune complex-mediated (IgA, SLE, endocarditis, etc)

No staining - pauci-immune (vasculites)

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140
Q

What is the difference between Goodpasture’s and anti-glomerulobasement membrane disease?

A

Renal limited: AGBM

Renal + lung: Goodpasture’s

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141
Q

What Ig is anti-GBM and Goodpasture’s?

A

IgG

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142
Q

What are the 6 renal lupus classifications?

A 
I: No or minimal changes
II: Mesangial glomerulitis
III: Focal, segmental glomerulonephritis
IV: Diffuse glomerulonephritis
V: membranous nephropathy
VI: Renal failure
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143
Q

2 mechanisms of hyperfiltration injury

A

Circulating factors

Mechanical stress

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144
Q

What 4 things are associated with membranous glomerulopathy 15% of the time?

A

Bugs - infections
Drugs - rheumatoid meds
Tumors
Rheum - SLE

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145
Q

What is the mechanism for membranoproliferative glomerulonephritis?

A

Subendothelial deposits cause injury to the endothelial cell

It retracts and puts a new layer of basement membrane between the deposit and itself

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146
Q

Is renal amyloidosis hypo or hypercellular?

A

Hypocellular - amyloid deposits wipe out the glomerulus and deposit in vessels

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147
Q

What does amyloidosis look like on EM?

A

Spilled spaghetti

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148
Q

What 2 kidney lesions does diabetes cause?

A

Hyaline arteriolar disease

Diabetic glomerulosclerosis

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149
Q

What happens in diabetic glomerulosclerosis?

A

Expansion of the mesangium
Basement membrane thickening

Mesangial lysis (they make so much basement membrane they kill themselves)

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150
Q

Wat is the gross appearance of the kidney in hypertensive renal disease?

A

Finely granular surface fromscarred glomeruli

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151
Q

What happens to the kidney in hypertensive renal disease (2)?

A

Medial and intimal thickening

yaline deposition

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152
Q

What happens in malignant/accelerated hypertensive renal disease?

A

Renal vasculature injury

  • > fibrinoid necrosis, hyperplastic arteriolitis (ok inflammation)
  • > increased renin
  • > viscious cycle
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153
Q

What is uremia?

A

Dysregulation of stuff when there is severe loss of all renal functions

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154
Q

3 other things that get fucked up when your kidney is really fucked

A

Erythropoietin -> anemia
Renin -> hypertension
Vitamin D -> osteomalacia

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155
Q

Within what time frame must urinalysis be done in?

A

2 hours of collection

Or refrigerated if longer (but less than 24 hours)

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156
Q

What can cause a false positive on a urinalysis glucose screen? A false negative?

A

Jar is left open

Vitamin C

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157
Q

What does nitrite in the urine mean?

A

Gram negative bacteria

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158
Q

What do hyaline casts indicate?

A

They are normal

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159
Q

Hypo and hypernatremia refer to the concentration of sodium where?

A

In the serum

NOT total body

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160
Q

Urine can be _____ times more concentrated than plasma

A

4

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161
Q

What 2 things does ADH/vasopressin do?

A

Increase renal water reabsorption

Vasoconstriction

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162
Q

What is hte most common electrolyte disturbance in hospitalized patients?

A

Hyponatremia

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163
Q

What is a common mechanism of hyponatremia? What are 2 ways this can occur?

A

Elevated serum osmolality from a solute other than sodium

Hyperglycemia
Mannitol/glycerol administration

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164
Q

2 conditions that cause isotonic hyponatremia

A

Lab artifact:
Hyperlipidemia
Hyperproteinemia (like multiple myeloma)

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165
Q

Explain lab artifact isotonic hyponatremia

A

Plasma osmolality is normal but there is less water content *because of hyperlipiedmia or hyperproteinemia)

It is a laboratory artifact of flame photometry and a sodium-sensitive electrode will yield a normal value

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166
Q

Deficiency in what hormone causes hypovolemic hyponatremia?

What about euvolemic hyponatremia?

A

Mineralocorticoid

Glucocorticoid

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167
Q

4 causes of hypervolemic hyponatremia

A

Congestive heart filaure
Hepatic cirrhosis
Nephrotic syndrome
Advanced chronic or acute renal failure

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168
Q

What is serum osmolality like in hypernatremia?

A

It is always increased

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169
Q

What is diabetes insipidus?

A

Excessive thurst and excretion of lots of dilute urine. Reuction of fluid intake does not concentrate urine

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170
Q

What are the 2 kinds of diabetes insipidus?

A

Central - ADH/vasopressin is not made

Nephrogenic - insensitiity to ADH/vasopressin

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171
Q

Equation for amount of water needed to treat someone with hypernatremia

A

0.6*body weight in kg * [actualNa/desiredNa-1]

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172
Q

What is effective arterial blood volume?

A

Volume of blood detected by volume sensors in the arteries

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173
Q

What are the 4 categories of volume sensors?

A

Low-pressure baroreceptors - veins
High-pressure baroreceptors - carotid and aortic body
Intrarenal sensors
Hepatic and CNS sensors

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174
Q

What is the end product of the RAAAS?

A

Aldosterone

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175
Q

4 substances that decrease sodium reabsorption

A

Natriuretic peptides
Prostaglandins
Bradykinin
Dopamine

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176
Q

4 substances that increase sodium reabsorption

A

Angiotensin II
Aldosterone
Catecholamines
Vasopressin/ADH

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177
Q

What does sympathetic stimulation do to natriuresis?

A

Increases sodium reabsorption

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178
Q

What are 3 ways Na gets reabsorbed in the distal colvoluted tubule?

A
  1. Na channels
  2. NaCal cotransporter
  3. Na/H antiporter

These are all on the luminal side

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179
Q

How does sodium get into the principal cells of the cortical collecting duct?

A

Na enters and is exchanged for K

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180
Q

What is Bartter’s syndrome? Where in the kidney is the defect?

A

A mutation in the Na/K/2Cl cotransporter in the thick ascending loop of Henle?

Hypokalemia
Hypomagnesemia
Metabolic alkalosis
High renin
High aldosterone
Increased calcium excretion
Normal blood pressure
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181
Q

What is Gitelman’s syndrome? Where in the kidney is the defect?

A

A mutation in the Na/Cl cotransporter in the distal tubule

Hypokalemia
Hypomagnesemia
Metabolic alkalosis
Reduced excretion of calcium

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182
Q

4 serum changes in stats of volume contraction

A

Increased BUN:plasma creatine ratio (>15)
Metabolic alkalosis if upper GI fluid loss
Metabolic acidosis if lower GI loss
Increased hematocrit and serum albumin

183
Q

6 diseases of nephrotic syndrome

A

Minimal change disease
Focal segmental glomerulosclerosis

Membranous nephropathy
Membranoproliferative nephropathy

Diabetes mellitus
Systemic amyloidosis

184
Q

What are 3 changes in cirrhosis that cause underfilling of the arterial circulation?

A

Hepatic and portal hypertension
Aplanchnic vasodilation
Hypoalbuminemia

185
Q

How does acetazolamide work?

A

Blocks carbonic anhydrase -> bicarb wasting -> metabolic acidosis and some diuretic action

Works in the proximal tubule

186
Q

How do loop diuretics work?

A

Inhibit Na/K/2Cl cotransporter in thick ascending limb

187
Q

How do thiazide diuretics work?

A

Inhibit the Na/Cl transporter
Blocking sodium entry
In distal convoluted tubule

188
Q

How do triamterene and amiloride diuretics work?

A

Sodium channel blockers in collecting duct

189
Q

How does spironolactone work?

A

Inhibits aldosterone

190
Q

What are 2 direct sodium channel blocker diuretics?

A

Triamterene

Amiloride

191
Q

How do the osmotic thresholds for thirs and ADH compare?

A

The threshold for thirst is a little higher (a few mOsm/kg)

192
Q

2 states that increase ADH. Which is stronger?

A

Hyperosmolality
Hypovolemia

Hypovolemia overrides if osmolality and volume are opposing

193
Q

3 causes of hypovolemic hyponatremia

A

Hemorrhage (due to rehydration without adequate Na intake)
Plasma volume and extracellular fluid losses
Decreased aldosterone as in addison’s disease

194
Q

3 causes of hypervolemic hyponatremia

A

CHF
Cirrhosis
(both these cause release of ADH due to reduced effective blood volume)

Severe renal failure (the kidneys can’t excrete water)

195
Q

Which type of diuretic impairs dilution and are a frequent cause of hyponatremia, particularly in the elderly?

196
Q

3 treatments for hypervolemic hyponatremia

A 
Water and salt restriction (giving salt is a frequent mistake but it worsens the edema!)
Loop diuretics (but not thiazides, which can worsen)
Inotropes if CHF
197
Q

What is the underlying cause of symptoms of hyponatremia? What are some of them (8)?

A

Cerebral edema

Anorexia, nausea, vomiting
Weakness, lethargy, confusion
Seizures, death

198
Q

If hyponatremia is chronic or uf unkonown duration, you slow correction to avoid what?

A

Central pontine myelinosis (osmotic demyelenation syndrome)

199
Q

3 things in treatment of euvolemic hyponatremia

A

Seizures -> hypertonic saline
Asymptomatic -> water restriction and correction of underlying disorder
ADH/vasopressin antagonists

200
Q

How does hypernatremia develop since we have a strong thirst reflex?

A

When patients don’t ave access to water

CNS problem that impairs thirst

201
Q

What are 2 things that can be mutated in congenital nephrogenic diabetes insipidus?

A 
AVP receptor (X-linked recessive)
Aquaporin 2 (autosomal R or D)
202
Q

How do you treat nephrogenic diabetes insipidus?

A

Vasopressin receptor antagonsts like tolvaptan

203
Q

What is the cause of gestational diabetes insipidus?

A

Release of vasopressinase from the placenta during the second half of pregnancy

204
Q

What is the job of the high-pressure baroreceptors?

A

Maintain mean arterial pressure by normalizing ECF volume

205
Q

What is glomerulo-tubular balance?

A

Changes in GFR induce a proportional change in the rate of proximal tubular sodium reabsorption

Part of renal autoregulation

206
Q

Where is most of the glomerular filtrate reabsorbed?

A

Proximal tubule

207
Q

How is the sodium gradient maintained in the proximal tubule? (so that sodium will go into the cell)

A

Na/K ATPase at the basolateral membrane puts sodium into the blood

208
Q

What does post-infectoius glomerulonephritis look like under imaging? (light, IF

A

Light microscopy - hypercellular, inflamed glomeruli
IF - granular
EM - large, subepithelial lump

209
Q

What are the 3 types of rapidly progressing glomerulonephritis?

A

They describe the immunoflourescence patterns

Linear - antibodies against the glomerular basement membrane

Granular - immune complex deposition

Pauci-immune - ANCA-positive vasculitis

210
Q

What is seen on urinalysis in acute tubular necrosis?

A

Brown granular casts

These were once the tubular cells

211
Q

3 endogenous substances that affect internal K balance

A

Insulin
Catecholamines (NE, epi)
Aldosterone (maybe and if so its role is small)

212
Q

What channel does K use to get out of the cells in the ascending limb of the loop of henle?

213
Q

Since aldosterone and cortisol bind to the mineralocorticoid receptor on cells in theascending limb of the loop of henle, how do we reduce the effects of cortisol?

A

Enzyme 11BOH-SDH turns cortisol into cortisone so it can’t bind

214
Q

What can cause a spirous low serum K? High serum K?

A

High WBC count

High platelet count

215
Q

How does hypomagnesia result in hypokalemia?

A

Mg prevents the K+ channel in the renal rubule from releasing potassium

Without Mg, renal K+ wasting occurs

216
Q

Are men or women more likely to have hypertension?

A

Their risks are equal

217
Q

Is systolic or diastolic blood pressure a more important cardiovascular disease risk factor in people over 50?

218
Q

What is the Guyton hypothesis of essential hypertension? (6)

A

Primary defect in renal sodium excretion from lower perfusion pressure

  • > increased plasma volume
  • > increased cardiac output
  • > overperfusion of organs
  • > autoregulatory increased in systemic vascular resistance
  • > increased blood pressure
219
Q

What is the cellular model of essential hypertension? (6)

A

In vascular smooth muscle cells

  • > Na/K ATPase inhibitor
  • > increased intracellular Na
  • > Na/Ca exchanger doesn’t work (it puts Na in and calcium out)
  • > SMC contracts
  • > increase in systemic vascular resistance
  • > increase in blood pressure
220
Q

What is the most important thing to do in hypertension management?

A

Stop smoking

221
Q

How do we define hypertension?

A

The level of blood pressure at which the benefits of therapy outweigh the risks

222
Q

How do you calculate mean arterial pressure?

A

(2*DBP + SBP)/3

223
Q

What are 3 proposed mechanisms of impaired natriuresis (the kidney excretes less Na than it should)

A
  1. Having less nephron mass -> decreased exretory ability
  2. Increased RAAS and sympathetic input -> more proximal tubular Na reabsorption
  3. Increased vascular resistance -> reduced renal blood flow
224
Q

What turns angiogensin I into angiotensin II?

A

ACE (angiotensin converting enzyme)

225
Q

What are 2 causes of renal artery stenosis? What are typical patient populaitons for each?

A

Fibromuscular dysplasia 50 years old and smokers and men

226
Q

2 clinical features that suggest primary hyperaldosteroneism

A

Hypokalemic metabolic alkalosis

Resistant hypertension

227
Q

What is the mineralocorticoid escape mechanism?

A

A mysterious mechanism where in hyperaldosteronism, sodium retention and edema don’t occur

228
Q

What is pheochromocytoma?

A

A benign tumor of the adrenal medulla that makes catecholamines

229
Q

What is a hypertensive crisis?

A

Acute management of elevated blood pressure plays a decisive role in outcome

230
Q

Why is determining if hypertensive neuroretinopathy is present important?

A

If present, it signifies a systemic hypertensive vasculopathy (with fibinoid necrosis and obliterative arteriopathy)

231
Q

What are the 2 findings that caracterize malignant hypertension?

A

Elevation of blood pressure

Widespread acute arteriolar injury

232
Q

What is the most characteristic feature of malignant hypertension? What causes it?

A

Cotton-wool spots on the fundoscopic exam

From ischemic infarction of retinal nerve fiber bundles

From proliferation of vascular endothelium -> occlusion

233
Q

What is goal blood pressure in patients with diabetes or chronic kidney disease?

234
Q

What drug class reduces hypertension by decreasing cardiac output and total peripheral resistance? Just CO? Just TPR?

A

Non-dihydropyridine calcium channel blockers (verapamil)

Beta blockers

Dihydropyridine calcium channel blockers (amlodipine)

235
Q

What drug classes reduces hypertension by decreasing cardiac output and total peripheral resistance?

A

Non-dihydropyridine calcium channel blockers

236
Q

Where is most of the body’s potassium?

A

Intracellular fluid

237
Q

What are 2 situations when K+ moves from intracellular fluid to the extracellular fluid?

A

Acidemia

Hyperosmolality

238
Q

How does insulin react to K+?

A

Their levels are proportional and dependent boht ways

Increased insulin moves K+ into cells

239
Q

How do beta-2 agonists affect K+?

A

Put K+ into cells

240
Q

How does exercise affect K+

A

Muscle inury

  • > leakage of K+ into extracellular fluid
  • > hyperkalemia

Athletes redistribute K+ into the muscles -> hypokalemia

241
Q

Which way does Na/K ATPase go?

A

3 Na out

2 Na in

242
Q

Where in the kidney do disorders of renal K+ handling occur?

A

Collecting duct

Either addition or reabsorption)

243
Q

Is adaptation to changes in Na or K intake faster?

244
Q

What is pH?

245
Q

What is the body’s normal pH range?

246
Q

What is ammonia trapping?

A

NH3 diffuses into the lumen
Binds H+
It becomes NH+, which can’t get back through the membrane of the tubule

247
Q

What size molecule does not pass through the glomerular filter?

A

60,000 daltons

248
Q

What prevents red blood cells from getting into Bowman’s space?

A

Fenestrated epithelium (the holes are too small)

249
Q

Where is the Na/K/2Cl cotransporter?

A

The thick ascending limb of Henle

250
Q

Where does ammonioagenesis occur?

A

Proximal tubule cells

251
Q

When is bicarbonate synthesized?

A

When there is no HCO3- in the tubular lumen

252
Q

What is the formulat for net acid excretion?

A

NH4+ excretion + titratable acid excretion - HCO3- excretion

253
Q

What is winter’s formula?

A

Expected CO2 = 1.5*bicarb + 8 +-2

TO see if appropriately respiratory compensaiton

254
Q

How do you tell if pH is being metabolically or respiratorily compensated for?

A

Compensation is the same way as the pH

Cause is the opposite way

255
Q

Where does mannitol work?

How does it work?

A

Proximal tubule

It is an osmotic diuretic

256
Q

5 adverse effects of loop diuretics

A 
Decreased K
Decreased Mg
Decreased hypocalcemia
Gout attack
Metabolic alkalosis
257
Q

When do you use ethacrynic acid?

A

When you want loop diuretic effects that aren’t sulfa drugs

258
Q

Where do loop diuretics work?

How do they work?

A

They inhibit the Na/K/2Cl cotransporter

259
Q

Where do thiazide diuretics work?

How do they work?

A

Distal tubule

Inhibit Na/Cl cotransporter

260
Q

What are 2 ways thiazide diuretics reduce hypertension?

A

Decrease plasma colume

Decrease cardiac output

261
Q

Thiazides can cause hyper_______ and hyper_______

A

Hypercalcemia

Hyperglycemia (in people with impaired glucose tolerance)

262
Q

How does chronic kidney disease alter thiazide diuretic response?

A

Thiazides become less effecteive because less drug reaches the site of action

You need a more effacious one at GFR

263
Q

How do potassium sparing diuretics work?

A

Bind to the aldosterone-dependent Na/K exchange site and prevent aldosterone from reabsorbing

264
Q

How do thiazides and loop diuretics affect uric acid?

A

They increase them

265
Q

Is there cross-reaction between sulfonamide antibiotics and diuretics?

266
Q

4 side effects of ACE inhibitors

A

Cough (from bradykinin not being broken down)
Hyperkalemia
Transient rise in serum creatinine
Angioedema

267
Q

3 side effects of ARBs

A

Hyperkalemia
Transient rise in serum creatinine
Angioedema

268
Q

Which calcium channel do CCBs block? What does this accomplish?

A

L-type

Arterial vasodilation -> decreased peripheral vascular resistance

269
Q

What are the 2 classes of calcium channel blockers? What is the difference in their effects?

A

Dihydropyridines - peripheral and cardiac vasodilators

Non-dihydropyridines - cardiac stuff (negative inotropic activity)

270
Q

Non-dihydropyridines inhibit what enzyme?

Dihydropyridines inhibit what enzyme?

A

CYP450

3A4. CYP450 is an isoenzyme of 3A4, whatever that means

271
Q

How do hydralazine and minoxidil work?

A

Increase intracellular cGMP

  • > relaxaiton of arterial smooth muscle
  • > decreased systemic pressure and contractility
272
Q

What is the suffix for alpha-1 receptor blockers?

A

-azosin

Terazosin
Doxazosin
Prazosin

273
Q

How do alpha-1 receptor blockers work? What are they used for?

A

Peipheral postsynaptic blockade

  • > decrease in arterial tone
  • > relaxes smooth muscle of bladder neck

They are used for BPH

274
Q

What are 2 alpha-2 receptor agonists we care about?

A

Clonidine

Methyldopa

275
Q

How does bone act as a buffer?

A

In acidosis, osteoblasts are suppressed and osteoclasts are stimulated

276
Q

Do we ingest/make an exces of acid or base?

277
Q

How does the kidney transport hydrogen into the urine?

A

Sodium-hydrogen exchanger

278
Q

What are the 2 main buffers in the urine?

A 
TItratable acids (complexing of a hydrogen ion toa filtered acid anion)
Ammonia
279
Q

How does hyper/hypokalmeia affect ECF pH?

A

Hypokalemia -> alkalosis

Low K+ causes H+ shif into cells
Increased H+ in tubule cells means more is excreted

High K+ causes H+ to be inappropriately retained in the ECF

280
Q

What is the bicarb equation?

A

H+ + HCO3- H2CO3 H2O + CO2

281
Q

That is the expected increase in bicarbonate in respiratory acidosis in acute and chronic settings?

A

Acute: dHCO2- increases by 1 mEq/L for every 10 mmHg increase in PCO2

Chronic: dHCO3 increases by 4 mEq/L for every 10 mm increase in PCO2

282
Q

What are the 2 steps of metabolic alkalosis?

A 
Generation
Miaintenance (always the kidney's fault)
283
Q

In what case do you give hypertonic saline?

284
Q

Why does ADH cause hyponatremia?

A

It causes reabsorption of water, not sodium

285
Q

Which diuretic can cause hyponatremia?

286
Q

What causes euvolemic hyponatremia?

A

Syndrome of inappropriate ADH secretion

287
Q

When do you give D5W?

A

For volume expansion in cases of low blood sugar or high sodium

288
Q

What does insulin do to potassium?

A

Shifts it intracellularly

289
Q

What does increased blood pH do to potassium?

A

Shifts potassium extracellularly

Because of the K/H exchanger

290
Q

IN what state are peaked T waves seen on an EKG?

A

Hypokalmia

291
Q

What does beta2 input do to potassium?

A

Shifts it intracellularly

292
Q

What is the effect of increased tubular flow on potassium secretion?

A

Increased tubular flow makes secretion easier (so, more) because the fluid goes away

293
Q

What is contraction alkalosis?

A

Loss of chloride-rich fluid

294
Q

How does chloride afect blood pH?

A

Chloride depletion results in resporption of bicarbonate by the kidney

Thus, it maintains metabolic alkalosis

295
Q

How does aldosterone contribute to alkalosis?

A

It induces H+ ATPase activity

296
Q

What are 2 causes of chloride-resistant metabolic alkalosis

A

Hyperaldosteronism

Cushing’s syndrome

297
Q

Equation for the expected increase in CO2 in metabolic alkalosis

A

dCO2 = (0.25 to 1.0)*HCO3

298
Q

How do you treat chloride-responsive acidosis and chloride-resistant alkalosis?

A

NaCl infusion or KCl

Block mineralocorticoid effect with spironolactone or amiloride

299
Q

How do you calculate a urine anion gap? What does it mean?

A

Na+K - Cl

Negative -> ammonia production in kidney is occuring

Positive -> renal ammonia production impaired an a renal tubular acidosis is present

300
Q

Is acetazolamide a sulfa drug?

301
Q

What is the results of inhbiting the Na/K/2Cl transporter with loop diureteics?

A

Medulary intersitium decreases tonicity

-> inhibition or reabsorption of water

302
Q

Can you use loop diuretics on edema caused by calcium channel blockers?

A

No

Only cardiovascular, renal, or hepatic disease

303
Q

3 adverse effects of spironolactone

A

Hyperkalemia
Gynecomastia
Amenorrhea

Eplerenone also does 1 and 3

304
Q

What are 2 sodium-channel blocker diuretics we care about?

A

Triamterene

Amiloride

305
Q

What is the suffix for ARBs?

A

-sartan

Angiotensin II receptor blockers

306
Q

What is the mechanism of action of calcium channel blockers?

A

L-type channel block

  • > less intracellular calcium in muscles
  • > inhibition of intracellular phosphodiesterase
  • > increased GMP
  • > inhibition of vascular SMC contractility and cardiac conduction
307
Q

What is the difference in target between dihydropyridines and nondihydropyridines?

A

Dihydropyridines are selective for L-type Ca channels in blood vessels

Non-dihydropyridines bind equally to cardiac and vascular L-type Ca channels

308
Q

What are 2 direct vasodilators we care about?

A

Hydralazine

Minoxidil

309
Q

How doe smnoxidil work?

A

Potassium chanel opener

-> hyperpolarizaiton of cell membranes

310
Q

How does hydralazine work?

A

Alters calcium metabolism messing up the contractility somehow of the vasculature

311
Q

What suffix is for alpha-1 blockers?

312
Q

How does clonidine work?

A

Stimulates alpha-2 adrenergic receptors

Decreases peripheral vascular resistance
Inhibits norepinephrine

313
Q

What is the difference between hypertensive urgency and emergency?

A

Urgency - severe elevation

Emergency - BP >180/120 with organ dysfunction

314
Q

How does sodium nitroprusside work?

A

Nitric oxide donor
Activates guanyl cyclase
-> myosin dephosphorylatin
-> VSMC relaxation

315
Q

Which hypertension drug is light-sensitive and requires reconstitution in a vial?

A

Sodium nitroprusside

316
Q

What is the definition of chronic kidney disease?

A

A permanent reduction in GFR

317
Q

6 causes of chronic kidney disease

A 
Diabetic nephropathy
Hypertensive nephrosclerosis/renal vascular disease
Glomerulonephritis
Polycystic kidney disease
Interstitial nephritis
Obstruction
318
Q

In chronic kidney disease, wthe rise of what 2 substances occurs to maintain balance?

A

FGF-23

Parathyroid hormone

319
Q

What is the most important factor in decreasing the progression of kidney disease?

A

Blood pressure control

320
Q

When is dialysis initiated?

A

When the risks of uremic complications exceed the risks of dialysis

321
Q

What are the 3 ways heodialysis can be sceduled?

A

3 times per week
Short daily
Nocturnal

322
Q

What are the 3 typical locations for arteriovenous shunts for hemodialysis?

A

Radiocephalic
Brachiocephalic
Brachiobasilic

323
Q

Where does a dialysis catheter go?

A

Inernal jugular (so it’s a port I think)

324
Q

3 limittions of dialysis

A

Uremia may not improve all the way
Difficult to remove enough volume to achieve euvolemia
Hperphosphatemia can ocure

325
Q

What is warm and cold ischemia for a kidney transplant?

A

Warm - time from cardiac death/clamping in doner

Cold - time from cold perfusion to recipient anastomosis (24-36 hours)

326
Q

What are the 2 pathways of T cell activation in transplant rejection?

A

Direct: Recipient T cells recognize intact donor HLA antiens on donor APCs

Indirect: recipient T cells recognize donor HLA antigen fragments on host APCs. This is the ‘normal’ mechanism of activation

327
Q

What happens to CD4 Th cells when actiated?

A

They differentiate nto various subtypes depending on the stimulus and environment

328
Q

Which 3 cytokines do TH1 cells make?

A

IFN-Y
TNF-a
IL-2

329
Q

Is Th1 or Th2 the dominant immune response in acute allograft rejection?

330
Q

Which cells is HLA class 1 on? HLA class II?

A

HLA/MHC 1 - all cells

HLA/MHC 2 - APCs

331
Q

What are the 2 modes of transplant rejection?

A

Cellular (T-cell)

Antibody (B cell)

332
Q

What are the 2 types of cellular kidney transplant rejection?

A

Tubulitis -> Banff class I

Vasculitis -> Banff class II

333
Q

3 criteria to determine if antibody-mediated kidney rejection is occuring

A

peritubular capillary C4d staining

Graft damage
Donor specific antibodies

334
Q

2 1st degree agents
2 second degree agents
3rd degree agents

For immunosuppression to limit immune graft damage

A

Calcineurin inhibitors cyclosporine, tacrolimus

Proliferation inhibitors MMF, sirolimus

Prednisone

335
Q

How do NSAIDS work?

A

They block cyclooxegenase 1 and 2, resulting in lack of prostaglandin and thromboxane production

336
Q

Which beta-blocker do we like to use in chronic kidney disease?

A

Metroprolol because its half-life is not prolonged

337
Q

4 drug classes that can causehyperkalemia in chronic kidney disease

A

POtassium-sparing diuretics
ACE inhibitors
ARBs
Digoxin

338
Q

6 things to give for hyperkalemia if EKG cheanges are present and their 3 different categories

A

To antagonize cardiac conduction abnormalities:
Calcium gluconate
Sodium bicarbonate

To shift K+ Intracellularly:
Glucose + insulin
Albuterol nebs (super hoigh doses)

To remove K+ from the body:
K exchange resin
Hemodialysis

339
Q

How does Kayexalate K+ exchange resin work?

A

Binds K+ in exchange for Na+ in the gut

340
Q

How does Patiromer/Veltassa K+ exchange resin work?

A

Exchanges Ca++ sorbitol for K+ in the gut

341
Q

What are the 5 stages of chronic kidney disease?

A 
1 - kidney damage, normal GFR
2 - kidney damage, mild GFR decrease
3 - moderate
4 -severe
5 - kidney failure

They all have GFR requirements

342
Q

Wt which CKD stage do you need to renally dose drugs?

343
Q

How do you deal with diuretic resistance in CKD?

A

Synergistically combine diuretics that act at different sites of the nephron

344
Q

How does serum phosphate affect serum calcium leels?

A

They are inversely proportional

High phosphate -> lowers calcium

345
Q

What is the trade-off hypothesis in chronic kidney disease?

A

kidney failure

  • > phosphorus is retained
  • > calcium is lowered
  • > parathyroid release
  • > excretino of phosphate and restoration of calcium levels

Eventually the renal tubules can no longer respond, bone disease occurs, and sytemic toxicity may happen

346
Q

How does the kidney compensate for hydrogen ions in CKD?

A

Increase in NH4+

347
Q

What are 4 reasons why anemia occurs in CKD?

A

Decreased erythropoietin
Shortened RBC lifespan, possibly due to a uremic toxin
Blood loss, possibly due to abnormal coagulation
Marrow fibrosis

348
Q

What are 3 reasons why hypertension occurs in CKD?

A

Expansino of extracellular fluid volume (reduce ability to excrete sodium)

Incresed RAAS

Autonomic dysfunction and baroreceptors are insensitive

349
Q

What is the number one thing to do to reduce CKD progression?

A

Treatment of hypertension with ACEIs or ARBs

350
Q

What is a disadvantage of a catheter vs arteriovenous fistula/graft? An advantage?

A

Disadvantage - infection, mostly Staph

Advantage is ready immediately vs. weeks

351
Q

Peritoneal dialysate has a lot of _____ to provide a high oncotic pressure

352
Q

Why doesn’t the unterovesice junction have a valve?

A

The ureter goes into the bladder at an angle and this works

353
Q

What are radio-paque stones made out of?
Semiopaque?
Not radiopaque (soo radiolucent?)

A

Radiopaque - calciu oxalate and phosphate

Semiopaque - magnesium ammonium phosphate

Other - uric acid, cystine

354
Q

5 risk factors for kidney stones

A

Hypercalcemia

Increased uric acid

Low pH

Decreased volume

Bacteria

355
Q

5 consequences of urinary tract obstruction

A

Hyeronephrosis, hydroureter

Infection

Chronic obstructive pyelonephritis

Renal failure

Hypertension

356
Q

What are the 2 parts of the female intrinsic urinary sphincter?

A

Bladder neck muscle fibers

Mid-urethral complex

357
Q

What are the 3 parts of the male intrinsic urinary sphincter?

A

Bladder neck circular muscle fibers

Smooth muscle of prostate and membranous urethra

358
Q

What are the effects of parasympathetic (1) and sympathetic action (2) on the bladder?

A

PS: detrusor contraction

S: inhibition of detrusor, increased tension in smooth muscle of bladder neck and proximal urethra

359
Q

What nerves are the somatic innervation of the bladder?

360
Q

Which 3 parts of the brain provide input to micturition?

A

Cortex (inhibitory)

Cerebellum and brainstm (facilitatory)

361
Q

What are the 5 steps of bladder emptying?

A

Storage
Emptying/voiding/micturition1. increase in bladder wall tension
2. Afferent input overcomes inhibitory signal
3. Pudendal nerve activity stops, external sphincter/pelvic floor relaxes, detrusor neurons discharge
4. Proximal urethra opens
5. BLadder contracts

362
Q

What do hyperactive deep tendon reflexes suggest? Hypoactive deep tendon reflexes?

A

Hyper - upper motor nuerons are fucked

Hypo - lower motor neurons are fucked

363
Q

What drug class do you use to manage overactive bladder?

A

Antimuscarinic agents

They inhibit involuntary bladder contractions and increase bladder capacity

364
Q

4 side effects of antichoenergic therapy

A

Dry mouth
Constipation
Blurred vision
Drowsiness

365
Q

Do drugs for urinary incontinence affect the afferent or efferent nerves?

366
Q

What is the goal of medical management of stress urinary incontinence? What are the 2 drug classes?

A

Goal is to increas bladder outlet resistance

Alpha agonists
Estrogen

367
Q

What is the most common cause of pediatric hydronephrosis?

A

Uteropelvic junction obstruction

368
Q

What is the most common renal abnormality?

A

Ureteral duplication

369
Q

What is a ureterocele? Why is it a problem?

A

A cystic dilation of the part of the ureter that is within the bladder (intravesical part)

Can be obstructive or cause reflux

370
Q

Where does the urachus go?

A

From the dome of the fetal blader to the allantois of the umbilical cord

It forms the median umbilical ligament after birth

371
Q

What causes posterior urethral valves?

A

There are not supposed to be valsces there
They are from abnormal insertion of mesonephric duct on the cloaca before it divides into the urogenital sinus and anorectal canal

372
Q

What is hypospadias? What is epispiadias?

A

Hypospadias is when the orifice of penile urethra is somewhere along the ventral aspect of the penis (the part facing forward when penis is erect)

Epispadias is when it is on

It is from abnormal fusion of urogenital folds from androgen insufficiency

373
Q

What is chordee?

A

A fibrous band on the penis, causing it to curve

374
Q

What is exstrophy?

A

Exposure of the bladder mucosa b/c abdominal wall is absent

375
Q

What causes an exstrophy-epispadias complex?

A

Failure of separation of the primitive cloaca by the urorectal septum

376
Q

What are the 5 parts of Potter sequence?

A 
Renal agenesis
Small amt of amniotic fluid
Squished face
Amnion nodosum 
Pulmonay hyupoplasia
377
Q

What causes amnion nodosum? Why is ist bad?

A

Nodules of squamous cells on amniotic membrane b/c the baby sheds them.

Over time this erodes the surface of the amnion

378
Q

What is the cause of death in renal agenesis?

A

Respiratory insufficiency (Potter sequence)

379
Q

What causes prune belly/Eagle-Barrett syndrome?

A

Atrophy of anterior abdominal muscles due to megalocystis

380
Q

Which kidney is less likely to form?

A

The left one is more comonly absent

381
Q

What is renal ectopia? What are 2 complications?

A

When the kidney is not in the right place

May result in ureteral obstruction or discoid shape

382
Q

Where are kidneys usually fused in horseshoe kidney? What is the most common complication?

A

They are usually fused at the lower pole

Increased incidence of urolithiasis

383
Q

Which type of polycystic kidney disease presents earlier?

A

Autosomal recessive

384
Q

What is the most common cause of renal cysts?

385
Q

What other 5 organs can autosomal dominant polycystic kidney disease affect?

A 
Hepatic cysts
Mitral valve prolapse
Diverticulosis
Cerebral aneurisms (berry aneurisms)
Pancreatic cysts
386
Q

Where are the cysts in autosomal dominant PKD? Where are they in ARPKD?

A

AD - entire nephron

AR - collecting tubules

387
Q

What happens to the liver in autosomal recessive polycystic kidney disease?

A

Portal hypertension from bile duct proliferation and periportal fibrosis

388
Q

What causes multicystic dysplastic kidney?

A

Abnormal induction of metanephric blastema by uretal bud

389
Q

What happens to a multicystic dysplastic kidney after birth?

A

If is nonfunctional, asymptomatic, and will involute over time

390
Q

What is tubule cuffing on histology associated with?

A

Multicystic dysplastic kidney

391
Q

What are 3 pediatric kidney tumors?

A

Congenital mesoblastic nephroma

Wilms tumor

392
Q

What are the 3 components of a Wilms tumor?

A

Blastemal (small round blue cells)
Epithelial (tubules)
Stromal (fibroblastic)

393
Q

What is associated with worse prognosis in Wilms tumor? Describe. Why is this bad?

A

Anaplasia

These are large, hyperchromatic cells with weird mitotic figures

It means these tumors are less chemosensitive

394
Q

What is the stage of a bilateral Wilms tumor?

A

V (even though most cancers only go up to stage IV)

395
Q

4 components of Beckwith-Weidemann syndrome

A

Wilms tumor
GIgantism
Macroglossia
Abdominal wall defects

396
Q

4 components of WAGR syndrome

A

Wilms tumor
Aniridia (no iris)
Genitourinary malformation
mental Retardation

397
Q

Which kidney is used for transplant?

A

Left because the renal vein is longer

398
Q

Where do the renal vein and artery anastomosed to in a kidney transplant? Which side does the kidney go on?

A

External iliac vein and artery, usually on the right side

399
Q

Which MHC do CD8+ cells respond to?

400
Q

Which MHC do CD4+ cells respond to?

401
Q

Which MHC/HLA is on all nucleated cells?

402
Q

What are the 4 steps of T cell receptor activation?

A

Increased intracellular Ca2+ activates calmodulin

  • > Calmodulin binds/activates calcineurin
  • > calcineurin dephosphorylates nuclear transcription factor NFAT
  • > NFAT induces cytokine transcription in the nucleus (IL-2)
403
Q

What are the 3 steps of T cell proliferation after activation?

A

IL-2 and IL-15 activate JAK/STAT pathway

  • > mTOR pathway
  • > Nucleotide synthesis and cell cycle activation leading to clonal expansion
404
Q

What are the 3 classifications of kidney donors?

A

Standard
Donation after cardiac death
Extended criteria

405
Q

What are 2 inhibitors of T cell proliferation?

A 
Myocphenolate mofetil
mTOR inhibitors (siroliumus, everolimus)
406
Q

What does the urinary tract consti of?

A

Real pelvis
Ureter
Bladder

407
Q

What are the 2 routes of infection for a UTI?

A

Hematogenous

Ascending

408
Q

What is the most common cause of ascending UTI?

409
Q

What do “O” antigens mean?

A

They make certain E. coli strains more resistant

410
Q

What are the 3 kidneys in the embryo? What are the time points associated with each?

A

Pronephros (4 weeks)
Mesonephros (4 weeks-2 months)
Metanephros - 5 weeks - maturity)

411
Q

All 3 kidney stages develop from the ________ within the ________

A

Nephrogenic cord

Urogenital ridge

412
Q

What are the little bits of emryological kidneys within each somite called?

A

Nephrotomes

413
Q

What is the joining of the nephrotomes called?

A

Mesonephric duct

414
Q

The mesonephric duct is also called the _____

A

Wolffian duct

415
Q

What does the mesonephric duct/Wolffian duct become?

A

Epididymus

Vas deferens

416
Q

The paramesonephric duct is also called the ______

A

Mullarian duct

417
Q

What does the paramesonephric duct/Mullerian duct become?

A

Oviducts and uterus parts

418
Q

The Mullerian duct is also called the ______

A

Paramesonephric duct

419
Q

Whe wolffian duct is also called the _______

A

Mesonephric duct

420
Q

The ______ surrounds the ureteric bud

A

Metanephric blastema

421
Q

What 4 things does the metanephric blastema become?

A

Ureter
Renal pelvis
Major calyces
Minor calyces

422
Q

3 benign tumors of the kidney

A

Renal papillary adenoma
Angiomyolipoma
Oncocytoma

423
Q

3 cell types in clear cell renal cell carcinoma

A

Clear
Granular
Spindle

424
Q

What genetic disease is associated with Clear cell renal cell carcinoma?

A

Von Hippel-Lindau disease

425
Q

What are the 4 renal cell carcinomas?

A

Clear cell
Chromophobe
Collecting duct
Familial

426
Q

4 exposers that increase risk of transitional urinary tract cancers

A

Smoking
acrylamide
Schistosoma haematobium
Radiation

427
Q

What is medullary sponge kidney?

A

A congenital disorder where cystic dilation of collecting tubules occurs

428
Q

Autosomal dominant PDK is due to a defect in which protein? What is autosomal recessive PDK due to?

A

Polycystin

Fibrocystin

429
Q

What is nephrophthisis-medullary cystic kidney disease complex?

A

A heritable disease where medullary cells die

430
Q

In kidney failure how does an increased in volume of distribution affect
drug plasma concentration? A decreased volume of distribution?

A

They both increase plasma concentration

So, renal dosing usually means reduce med

431
Q

What 2 drugs dilate the affsorium Naerent arteriole? Which drug constricts it?

A

Dopamine, caffeine

NSAIDS

432
Q

What 2 drugs constrict the efferent arteriole?

A

ACEIs, ARBs

433
Q

How do you calculate FENa?

A

urinary Na * plasma creatinine/(plasma Na*urinary creatinine)

434
Q

What can cause peaked T waves?

A

Hyperkalemia

435
Q

What electrolyte imbalance can lead to rhabdomyolysis?

A

Hypokalemia

436
Q

What is the equation for renal clearance?

A

Urine concentration * urine flow/plasma concentration

437
Q

What does angiotensin II doe to the glomerulus? What results does this have?

A

It vasoconstricts the afferent and efferent arterioles (but mostly the efferent)

This results in decreased GFR

438
Q

What does the macula densa respond to?

A

Changes in NaCl delivery

439
Q

Which hormone inserts aquaporins?

A

Aldosterone

440
Q

Is the response to ADH or aldosterone faster?

A

ADH, since it prompts vesicle fusion and aldosterone goes all the way to the nucleus to induce transrption of Na+ channels and pumps

441
Q

Is BUN/creatinine reabsorbed/secreted?

A

BUN is reabsorbed and creatinine is secreted

442
Q

How long after infection does post-infectious glomerulonephritis occur?

443
Q

What is the treatment for post-infectious glomerulonephritis?

A

Supportive

444
Q

What is a bad complication of PIGN in adults?

A

Can become RPGN

445
Q

What characterizes rapidly progressive glomerulonephritis?

A

Crescents in bowman’s space on H&E

This is fibrin and macrophages

446
Q

How do you differentiate types of post-infectious glomerulonephritis

A

Immunoflourescence

447
Q

Which disease results in thinning and splitting of the glomerular basement membrane?

A

Alport syndrome

448
Q

What part of the kidney is renal cell carcinoma from?

A

Kidney tubules

449
Q

What is the classic symptomatic triad in renal cell carcinoma?

A

Hematuria
Palpable mass
Flank pain

450
Q

Where does the uteric bud branch from?

A

The mesonephric duct

451
Q

How many people in the US have hypertension?

A

50-60 million

452
Q

What does the Furnman criteria apply to?

A

Clear cell carcinoma

453
Q

What is the fate of the ureteric bud? The metanephric blastema?

A 
Urinary tract (urethra to tubules)
Kidney

Spring 2016 - CVPR (4 decks)

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