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NURA 662 Adv Pathophysiology > Renal > Flashcards

Renal Flashcards

1
Q

Normal renal functions

A
  • maintain water balance –> ultimately manages BP
  • regulate the quantity and concentration of ECF ions (consider the net handling of Na, Cl, K, Ca, etc when kidneys are not working properly)
  • maintain plasma volume
  • acid base balance – (may have acidosis, inability to excrete acids)
  • excrete waste products (high levels of BUN, creatinine)
  • secretion of renin, erythropoietin, etc. (may see anemia, BP dysregulation)

CONSIDER HOW FAILURE OF THESE FUNCTIONS OF THE KIDNEY WILL MANIFEST

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2
Q

Which types of cells lay down the glomerular basement membrane?

A

mesangial cells - modified smooth muscle cells (ability to contract) that filter based on charge

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3
Q

GFR is dependent on which factors?

A
  • Kf = surface area
  • hydrostatic pressure of capillary - comes from BP (ONLY FACTOR THAT FAVORS FILTRATION)
  • oncotic pressure of capillary (opposes filtration)
  • hydrostatic pressure of bowmans space (under normal conditions, very small, ALMOST a constant)
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4
Q

Kidney disease is America’s ____ leading cause of death.

A

9th

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5
Q

_________ is the 2nd leading cause of RF.

A

High blood pressure

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6
Q

45% of kidney failure is caused by ________.

A

diabetes

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7
Q

Acute renal failure: defined

A

sudden decrease in GFR, resulting in an inc in the plasma conc of waste products (azotemia) normally excreted by the kidneys

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8
Q

ARF: manifestations

A

sudden loss of renal function characterized by:

  • reduced production of urine, oliguria or anuria
  • retention of H2O, H+, and minerals, resulting in metabolic acidosis
  • retention of metabolic waste products in the blood, most notably BUN and creatinine
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9
Q

Pathogenesis and specific causes of Pre Renal ARF

A

Any process that sharply decreases RENAL PERFUSION

  • hypotension
  • volume depletion (fluid loss, bleeding, etc.)
  • Primary cardiac pump failure –> hypotension
  • decreased SVR (sepsis)
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10
Q

Response to renal hypoperfusion

A
  • dec GFR –> inc ang II, inc ADH, inc aldosterone
  • Na and water retention
  • inc BUN/creatinine levels (inc BUN to creatinine ratio)
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11
Q

Treatment of pre renal failure

A

IMPROVE RENAL PERFUSION

  • volume replacement
  • dialysis
  • fix the underlying problem (sepsis, HF, etc.)

REMEMBER: there is nothing WRONG with the actual kidney, just hypoperfusion of the kidney

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12
Q

Postrenal ARF: causes

A

Tubular obstruction
-insult (ischemia) causes sloughing of cells and cast formation. Obstruction in the tubule then causes a retrograde increase in pressure and reduces the GFR

Tubular back-leak
-backward flow of filtrate

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13
Q

Postrenal ARF: early phase

A
  • reflex adaptation to maintain GFR despite rising tubular hydrostatic pressure
  • afferent arteriolar dilation, enhances glomerular perfusion
  • this phases lasts only 12-24 hours
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14
Q

Postrenal ARF: late phase

A
  • after 12 - 24 hours, the afferent vasodilation ceases
  • progressive fall of renal perfusion: glomerular blood flow and GFR drop
  • may result in anuria!
  • continues until the obstruction is relieved

if prolonged, the ischemia leads to progressive permanent nephron loss

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15
Q

Postrenal ARF: recovery phase

A

AFTER RELIEF OF THE URINARY OBSTRUCTION

  • with release of the pressure, the pre renal vessels relax, perfusion is restored, and GFR increases in the nephrons which survive
  • tubular pressure returns to normal
  • HYDRONEPHROSIS - dilation of calyces and collecting system may remain permanently
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16
Q

BUN/Creatinine ratio >20/1: location of ARF and mechanism

A

Pre renal

reduced blood flow causes elevated creatinine and BUN. Additionally, BUN reabsorption is increased because of the lower flow; BUN is disproportionately elevated related to creatinine

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17
Q

BUN/Creatinine ratio 10-20/1: location of ARF and mechanism

A

Post renal

normal range

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18
Q

BUN/Creatinine ratio <10/1: location of ARF and mechanism

A

Intra renal

renal damage causes reduced reabsorption of BUN, therefore lowering the BUN/Cr ration

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19
Q

Chronic Renal Failure: defined

A

gradual and progressive loss of the ability of the kidneys to excrete wastes, concentrate urine, and conserve electrolytes due to diseases affecting the kidney either

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20
Q

Primary causes of chronic renal failure

A

chronic glomerulonephritis

interstitial nephritis

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21
Q

Secondary causes of chronic renal failure

A

hypertensive vascular disease
diabetes
partial urinary tract obstruction

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22
Q

Progression of CRF

A

reduced renal reserve
renal insufficiency
renal failure
end stage renal failure

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23
Q

Progression of CRF: Renal insufficiency manifestation

A

mild azotemia, nocturia, mild anemia

GFR reduced

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24
Q

Progression of CRF: Renal failure manifestation

A

azotemia, acidosis, impaired urine dilution, severe anemia, hypernatremia, and hyperkalemia

GFR below 20% (lost 80% of nephrons)

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25
Q

Progression of CRF: end stage renal failure

A

all organ systems affected

near absence of GFR

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26
Q

What is uremia?

A

refers to a number of symptoms caused by a decline in renal function with the accumulations of toxins
–causes unknown, and It appears that urea and creatinine build up plays little to no role

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27
Q

S/S of uremia

A 
anorexia
nausea
vomiting
diarrhea
weight loss
edema
neurologic changes
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28
Q

CRF: calcium balance

A
  • vitamin D levels decrease
  • diminished absorption of calcium from the gut

plasma phosphate levels increase because of the decrease in GFR and inability to secrete phosphate
-so not only are we not absorbing as much calcium from the gut, but we are binding more calcium in the blood because there is more phosphate

-overproduction of parathyroid hormone!

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29
Q

CRF: sodium and water balance

A
  • sodium must be regulated within narrow limits
  • nephron is very efficient at reabsorbing Na
  • when GFR declines, a decreased fraction of filtered Na and water must be reabsorbed – keeps them in balance
  • CRF kidneys become less flexible
  • urinary dilution and concentration are impaired
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30
Q

CRF: potassium balance

A

-aldosterone - mediated potassium transport unable to function at such a lower GFR

remember potassium is normally SECRETED

–hyperkalemia results!!

-the risk increases as the disease progresses and must be controlled by dialysis

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31
Q

CRF: acid base balance

A

remember kidneys normally secrete acids in large amounts

  • as the kidney fails, ammonia synthesis decrease
  • there is compensation, but must be treated with dialysis if severe
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32
Q

CRF, renal osteodystrophy: manifestations

A
  • elevated serum phosphate levels
  • decreased serum calcium levels
  • impaired activation of vitamin D
  • hyperparathyroidism

can lead to brittle bones over time

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33
Q

CRF, hematologic alterations: manifestations

A

-decrease in the production of erythropoietin, thus an inadequate production of RBC

  • normochromic - normocytic anemia
  • –blood cells themselves are normal, size and shape are normal, enough hgb on cell, just don’t have enough cells

-anemia presents with: lethargy, dizziness, low hct

  • left ventricular hypertrophy
  • -because we have a lower carrying capacity, heart is going to work harder to get out small amouts of O2
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34
Q

CRF, CV system: manifestations

A
  • HTN resulting from excess fluid volume and Na levels
  • –from elevated renin
  • dyslipidemia
  • constitutes the most frequent cause of death in this population
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35
Q

CRF, neural function: manifestations

A
  • mild sleep disorders, impaired concentration, memory loss, and impaired judgement may occur in some individuals
  • some may experience frequent hiccups, muscle cramps and twitching
  • caused by alterations in electrolyte and metabolic product elevation
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36
Q

CRF, endocrine function and reproduction: manifestations

A
  • uremic males and females have a decrease in sex steroids
  • —-amenorrhea and inability to maintain a pregancy in females
  • —-decreased libido and impotence in men, and sometimes infertility

cause not entirely known

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37
Q

CRF, immunologic dysregulation: manifestations

A
  • generalized immunosuppression due to unknown reasons
  • increases susceptibility to infection
  • deficient response to vaccination
  • impaired wound healing

–dialysis needed!

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38
Q

CRF, GI function: manifestations

A
  • non specific GI complications including: anorexia, nausea and vomiting, along with a metallic taste in the mouth (nitrogenous waste products being broken down by saliva in mouth)
  • uremic gastroenteritis: bleeding ulcerations along mucosa that results in significant blood loss
  • uremic fetor: form of bad breath caused by urea breakdown by salivary enzymes
  • symptoms alleviated when dietary protein is restricted OR institution of regular dialysis
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39
Q

CRF: treatment besides dialysis and transplant list

A
  • preserve remaining nephron function (figure out what is causing RF and STOP IT)
  • dietary management (low K, low protein, low phos intake, low acid)
  • Na and fluid management
  • erythropoietin
  • control hypertension
  • careful prescribing of drugs that are potentially nephrotoxic
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40
Q

Azotemia definition

A

elevation of BUN and Cr levels: related to decrease in GFR

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41
Q

Azotemia s/s

A 
decreased or absent urine
fatigue
decreased alertness
confusion
pale skin
tachycardia
dry mouth
thirst
swelling
orthostatic BP
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42
Q

Uremia definition

A

when azotemia is combined with other clinical symptoms and biochemical abnormalities.

signs of failing excretory system and other metabolic and endocrine abnormalities

broader term referring to the pathological manifestations of severe azotemia.

Includes azotemia, acidosis, hyperkalemia, HTN, anemia, hypocalcemia along with other findings

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43
Q

Mechanism of glomerular injury related to inflammation: endogenous antigen

A

immune system will recognize something within the glomerulus as being foreign and start attacking

tends to be more severe than exogenous

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44
Q

Mechanism of glomerular injury related to inflammation: exogenous antigen

A

antigen can come from somewhere else in the body and initiate inflammation

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45
Q

Nephrotic syndrome symptoms: CHAPPED

A 
C oagulability (hyper)
H yperlipoproteinuria
A lbuminemia (hypo)
PP roteinuria (double P because there is a lot of protein lost in urine including immunoglobulins
E dema
D yslipidemia
46
Q

Membranous glomerulonephritis: population

A

adults, most commonly in 6th decade or older

47
Q

Membranous glomerulonephritis: histologic changes

A

-thickening of glomerular basement membrane

48
Q

Membranous glomerulonephritis: mechanism/etiology

A

How is this happening??

ENDOGENOUS immune complex

49
Q

Membranous glomerulonephritis: S/S

A

NEPHROTIC SYNDROME

50
Q

Membranous glomerulonephritis: treatment

A
  • immunomodulators

- -*RESPONDS WELL TO STEROIDS

51
Q

Membranoproliferative Glomerulonephritis: population

A

Any age group

52
Q

Membranoproliferative Glomerulonephritis: mechanism/etiology

A

EXOGENOUS immune complex

antigen from “somewhere else” floating in plasma, antibody will bind to it, form a complex, then deposit itself into glomerulus - immune complex will initiate immune response

53
Q

Membranoproliferative Glomerulonephritis: histologic changes

A

proliferation of cell type - mesangial cells (increase in mesangial cells cause a new layer of GBM –> tram track appearance)

inflammation/thickening of GBM

54
Q

Membranoproliferative Glomerulonephritis: s/s

A

NEPHROTIC SYNDROME

55
Q

Membranoproliferative Glomerulonephritis: treatment

A

Immunomodulators

–RESPONDS WELL TO STEROIDS

56
Q

Minimal change disease: population

A

most common in young children (2-6), more common in males

57
Q

Minimal change disease: mechanism/etiology

A

usually after a recent respiratory infection or after receiving routine immunizations

unknown etiology:

  • potentially a change in GBM charge
  • –causes fusion of foot processes (foot processes are NORMALLY negatively charged and repel each other which is why they can interdigitate and NOT clump together. It’s thought that maybe the immune response causes a “change in charge”)
58
Q

Minimal change disease: treatment

A

steroids

59
Q

Minimal change disease: s/s

A

Nephrotic syndrome starting with a “changed charge of the GBM”

60
Q

Focal segmental glomerulosclerosis: population

A

Idiopathic

  • sickle cell disease
  • cyanotic heart disease
  • IV drug abuse
61
Q

Focal segmental glomerulosclerosis: s/s

A

Nephrotic syndrome starting with “sclerosis” WITH:

  • presence of HTN
  • decreased renal function
62
Q

Focal segmental glomerulosclerosis: treatment

A

No known treatment

does not respond to immunomodulators

63
Q

Diseases associated with nephrotic syndrome

A

minimal change disease (lipoid nephrosis)

membranous glomerulonephritis (membranous neuropathy)

focal segmental glomerulosclerosis

membranoproliferative glomerulonephritis

64
Q

Nephritic syndrome s/s: “pharoh”

A

P roteinuria (less than nephrotic syndrome)
H ematuria
A zotemia (rise in nitrogenous waste products – metallic taste in mouth, inc BUN/Cr)
R BC cast
O liguria
H ypertension

65
Q

Nephritic syndrome disorders

A 
IgA nephropathy (Berger disease)
--most common in the world

Acute, proliferative (poststreptococcal, postinfectious) glomerulonephritis

66
Q

Post-streptococcal glomerulonephritis: mechanism/etiology

A 
streptococcal infection (outside the kidney) leads to immune complex formation
-pharyngitis or skin infection
67
Q

Post-streptococcal glomerulonephritis: s/s

A

nephritic syndrome

  • malaise
  • nausea
  • dark urine
  • oliguria
  • azotemia
  • edema
  • hematuria
68
Q

IgA nephropathy (Berger disease): population

A

can be anyone, but more common in children

69
Q

IgA nephropathy (Berger disease): histologic changes

A

presents with VAST DEPOSITS in the mesangium of the glomerulus

70
Q

IgA nephropathy (Berger disease): mechanism/etiology

A

often preceded by an infection associated with the mucosum

71
Q

Most common glomerular renal disease throughout the world

A

IgA nephropathy

72
Q

IgA nephropathy (Berger disease): s/s

A

nephritic syndrome

73
Q

IgA nephropathy (Berger disease): treatment

A

treated with immunomodulators

–steroids

74
Q

What is chronic glomerulonephritis?

A

final stage of MANY DIFFERENT FORMS OF GLOMERULONEPHRITIS, but often the kidney is so badly damaged that it is impossible to determine the type of glomerulonephritis that was the forerunner

75
Q

common symptom of chronic glomerulonephritis

A

HTN

76
Q

chronic glomerulonephritis: histological changes

A
  • microscopically the glomeruli are solidified either partially or wholly
  • tubules show much loss and atrophy, and arteries show intimal thickening
  • interstitium shows fine fibrosis and contains variable numbers of inflammatory cells
77
Q

Hematogenous infection: what is it? frequency?

A

less common

results from seeding of the kidneys due to septicemia or bacterial endocarditis

78
Q

Vesicoureteral reflux

A

occurs more readily with an urethral obstruction or cystitis as the urinary bladder pressure is increaed and the normal vesicoureteral valve is compromised

79
Q

How does a tubular injury cause decreased glomerular filtration?

A
  • back leak of filtration across damaged epithelium
  • decreased renal blood flow
  • decreased filtration properties of glomerulus
80
Q

Pyelonephritis: defined

A

infection, either ascended from the bladder or through the bloodstream

81
Q

Pyelonephritis: s/s

A 
chills
fever
HA
back pain
tenderness
general malaise
bladder irritators - dysuria, frequency, urgency
82
Q

chronic pyelonephritis: histologic changes

A

-dilated calyces, reflecting hydronephrosis

83
Q

chronic pyelonephritis: etiology

A

urine outflow obstruction of any kind with superimposed ascending infection

“deranged vesicoureteral junction”

recurrent infection results in inflammation and scarring of the renal parenchyma

84
Q

benign nephrosclerosis: etiology

A

may naturally occur with age as a result of years of mild, uncontrolled chronic HTN

progresses slowly, so symptoms may not be noticed unless the condition progresses to malignant nephrosclerosis

85
Q

benign nephrosclerosis: s/s

A

progresses slowly, so symptoms may not be noticed unless the condition progresses to malignant nephrosclerosis

seldom associated with significant proteinuria or inc serum Cr or reduced renal function

86
Q

benign nephrosclerosis: treamtent

A

anti hypertensive therapy

if uncontrolled, will lead to chronic renal failure

87
Q

benign nephrosclerosis: histologic changes

A

sclerosis of renal arterioles and small arterioles

few glomeruli may undergo ischemic wrinkling

88
Q

malignant nephrosclerosis: defined

A

DBP >130 mmHg - seen in 5% of patients w/ HTN of any cause

progresses very quickly and the damaged arteries are unable to provide enough oxygen to the kidney tissues, resulting in ischemic renal injury and RF.

89
Q

malignant nephroslerosis: associated s/s, conditions

A

associated with encephalopathy, retinopathy, CV abnormalities and RF

associated with significant proteinuria and azotemia

90
Q

malignant nephrosclerosis: treatment

A

aggressive anti hypertensive therapy

dialysis

91
Q

malignant nephrosclerosis: histologic changes

A

glomeruli: completely fibrotic

arteriole has “onion skin appearance” - thickening of the arterial wall is associated with a hyperplastic arteriosclerosis

92
Q

Leading cause of kidney failure

A

diabetes (T1 or T2)

93
Q

Diabetic nephropathy: main treatment once proteinuria is diagnosed

A

Keep BP <130/80

Most effective TX: ACE inhibitors or ARBs

94
Q

Diabetic nephropathy: histological changes

A 
glomerulosclerosis
tubulointerstitial fibrosis
arteriolar sclerosis (thick wall and narrow lumen)
95
Q

Adult polycystic kidney disease: heredity, population, and description

A

caused by AUTOSOMAL DOMINANT mutations in PKD 1-3 genes

usually non symptomatic until 3rd or 4th decade

96
Q

Adults polycystic kidney disease: manifestations

A

drop in kidney function –> CRF

significant HTN - 90% of deaths occur by CV events

97
Q

Adult polycystic kidney disease: description

A

leads to dilation in tubules (at any point), cysts are often seen in the liver and pancreas also

characterized by large cysts in one or both kidneys

98
Q

Autosomal recessive polycystic kidney disease: heredity and population

A

both parents but be carriers of the gene PKHD1

childhood polycystic kidney disease
-symptoms seen in utero and in the first few months of life

99
Q

autosomal recessive polycystic kidney disease: manifestions

A

HTN and decrease in urine concentrating ability is one of the most common early manifestations

high levels of Epo

100
Q

PKD: treatment

A

potential dialysis and then kidney transplant

101
Q

nephrolithiasis: defined

A

kidney stone found INSIDE kidney

102
Q

urolithiasis: defined

A

kidney stone that has exited the kidney and is now in the urinary tract

103
Q

Kidney stones are more common in men or women?

A

men

104
Q

hydronephrosis: common causes

A

stones in the renal pelvis

cancers fo the bladder, cervix, uterus, prostate, or other pelvic organs

105
Q

Most common renal neoplasm seen in adults

A

clear cell carcinoma

106
Q

Explain the name clear cell carcinoma

A

tubular cells accumulate glycogen and lipids, their cytoplasm appear “clear”, lipid laden

107
Q

clear cell carcinoma: manifestations

A

often presents with pain, as a palpable mass or with hematuria

may be clinically silent for year and may present with symptoms of metastasis, most commonly to the lungs!

108
Q

Wilms tumor: population

A

occurs in children, usually under age 5

109
Q

Wilms tumor: etiology

A

tumor usually arises as a result of failure of blastemal tissue to differentiate into normal renal structures

110
Q

Wilms tumor: manifestations

A

at the time of detection, wilms tumors are usually large

presents with pain due to size, fever, high BP, constipation

111
Q

Wilms tumor: TX

A

neoplasm is aggressive and metastasizes widely, but is responsive to surgery and chemotherapy.

NURA 662 Adv Pathophysiology (7 decks)

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