Renal Flashcards
(111 cards)
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
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
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)
4
Q
Kidney disease is America’s ____ leading cause of death.
A
9th
5
Q
_________ is the 2nd leading cause of RF.
A
High blood pressure
6
Q
45% of kidney failure is caused by ________.
A
diabetes
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
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
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)
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)
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
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
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
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
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
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
17
Q
BUN/Creatinine ratio 10-20/1: location of ARF and mechanism
A
Post renal
normal range
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
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
20
Q
Primary causes of chronic renal failure
A
chronic glomerulonephritis
interstitial nephritis
21
Q
Secondary causes of chronic renal failure
A
hypertensive vascular disease
diabetes
partial urinary tract obstruction
22
Q
Progression of CRF
A
reduced renal reserve
renal insufficiency
renal failure
end stage renal failure
23
Q
Progression of CRF: Renal insufficiency manifestation
A
mild azotemia, nocturia, mild anemia
GFR reduced
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)
25
Progression of CRF: end stage renal failure
all organ systems affected
near absence of GFR
26
What is uremia?
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
27
S/S of uremia
```
anorexia
nausea
vomiting
diarrhea
weight loss
edema
neurologic changes
```
28
CRF: calcium balance
- 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!
29
CRF: sodium and water balance
- 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
30
CRF: potassium balance
-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
31
CRF: acid base balance
**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
32
CRF, renal osteodystrophy: manifestations
- elevated serum phosphate levels
- decreased serum calcium levels
- impaired activation of vitamin D
- hyperparathyroidism
can lead to brittle bones over time
33
CRF, hematologic alterations: manifestations
-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
34
CRF, CV system: manifestations
- HTN resulting from excess fluid volume and Na levels
- --from elevated renin
- dyslipidemia
- constitutes the most frequent cause of death in this population
35
CRF, neural function: manifestations
- 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
36
CRF, endocrine function and reproduction: manifestations
- 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**
37
CRF, immunologic dysregulation: manifestations
- generalized immunosuppression due to unknown reasons
- increases susceptibility to infection
- deficient response to vaccination
- impaired wound healing
--dialysis needed!
38
CRF, GI function: manifestations
- 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
39
CRF: treatment besides dialysis and transplant list
- 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
40
Azotemia definition
elevation of BUN and Cr levels: related to decrease in GFR
41
Azotemia s/s
```
decreased or absent urine
fatigue
decreased alertness
confusion
pale skin
tachycardia
dry mouth
thirst
swelling
orthostatic BP
```
42
Uremia definition
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
43
Mechanism of glomerular injury related to inflammation: endogenous antigen
immune system will recognize something within the glomerulus as being foreign and start attacking
**tends to be more severe than exogenous**
44
Mechanism of glomerular injury related to inflammation: exogenous antigen
antigen can come from somewhere else in the body and initiate inflammation
45
Nephrotic syndrome symptoms: CHAPPED
```
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
Membranous glomerulonephritis: population
adults, most commonly in 6th decade or older
47
Membranous glomerulonephritis: histologic changes
-thickening of glomerular basement membrane
48
Membranous glomerulonephritis: mechanism/etiology
How is this happening??
ENDOGENOUS immune complex
49
Membranous glomerulonephritis: S/S
NEPHROTIC SYNDROME
50
Membranous glomerulonephritis: treatment
- immunomodulators
| - -*RESPONDS WELL TO STEROIDS
51
Membranoproliferative Glomerulonephritis: population
Any age group
52
Membranoproliferative Glomerulonephritis: mechanism/etiology
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
Membranoproliferative Glomerulonephritis: histologic changes
proliferation of cell type - mesangial cells (increase in mesangial cells cause a new layer of GBM --> tram track appearance)
inflammation/thickening of GBM
54
Membranoproliferative Glomerulonephritis: s/s
NEPHROTIC SYNDROME
55
Membranoproliferative Glomerulonephritis: treatment
Immunomodulators
| --RESPONDS WELL TO STEROIDS
56
Minimal change disease: population
most common in young children (2-6), more common in males
57
Minimal change disease: mechanism/etiology
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
Minimal change disease: treatment
steroids
59
Minimal change disease: s/s
Nephrotic syndrome starting with a "changed charge of the GBM"
60
Focal segmental glomerulosclerosis: population
Idiopathic
- sickle cell disease
- cyanotic heart disease
- IV drug abuse
61
Focal segmental glomerulosclerosis: s/s
Nephrotic syndrome starting with "sclerosis" WITH:
- presence of HTN
- decreased renal function
62
Focal segmental glomerulosclerosis: treatment
No known treatment
does not respond to immunomodulators
63
Diseases associated with nephrotic syndrome
minimal change disease (lipoid nephrosis)
membranous glomerulonephritis (membranous neuropathy)
focal segmental glomerulosclerosis
membranoproliferative glomerulonephritis
64
Nephritic syndrome s/s: "pharoh"
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
Nephritic syndrome disorders
```
IgA nephropathy (Berger disease)
--most common in the world
```
Acute, proliferative (poststreptococcal, postinfectious) glomerulonephritis
66
Post-streptococcal glomerulonephritis: mechanism/etiology
```
streptococcal infection (outside the kidney) leads to immune complex formation
-pharyngitis or skin infection
```
67
Post-streptococcal glomerulonephritis: s/s
nephritic syndrome
- malaise
- nausea
- dark urine
- oliguria
- azotemia
- edema
- hematuria
68
IgA nephropathy (Berger disease): population
can be anyone, but more common in children
69
IgA nephropathy (Berger disease): histologic changes
presents with VAST DEPOSITS in the mesangium of the glomerulus
70
IgA nephropathy (Berger disease): mechanism/etiology
often preceded by an infection associated with the mucosum
71
Most common glomerular renal disease throughout the world
IgA nephropathy
72
IgA nephropathy (Berger disease): s/s
nephritic syndrome
73
IgA nephropathy (Berger disease): treatment
treated with immunomodulators
| --steroids
74
What is chronic glomerulonephritis?
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
common symptom of chronic glomerulonephritis
HTN
76
chronic glomerulonephritis: histological changes
- 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
Hematogenous infection: what is it? frequency?
less common
results from seeding of the kidneys due to septicemia or bacterial endocarditis
78
Vesicoureteral reflux
occurs more readily with an urethral obstruction or cystitis as the urinary bladder pressure is increaed and the normal vesicoureteral valve is compromised
79
How does a tubular injury cause decreased glomerular filtration?
- back leak of filtration across damaged epithelium
- decreased renal blood flow
- decreased filtration properties of glomerulus
80
Pyelonephritis: defined
infection, either ascended from the bladder or through the bloodstream
81
Pyelonephritis: s/s
```
chills
fever
HA
back pain
tenderness
general malaise
bladder irritators - dysuria, frequency, urgency
```
82
chronic pyelonephritis: histologic changes
-dilated calyces, reflecting hydronephrosis
83
chronic pyelonephritis: etiology
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
benign nephrosclerosis: etiology
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
benign nephrosclerosis: s/s
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
benign nephrosclerosis: treamtent
anti hypertensive therapy
if uncontrolled, will lead to chronic renal failure
87
benign nephrosclerosis: histologic changes
sclerosis of renal arterioles and small arterioles
few glomeruli may undergo ischemic wrinkling
88
malignant nephrosclerosis: defined
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
malignant nephroslerosis: associated s/s, conditions
associated with encephalopathy, retinopathy, CV abnormalities and RF
associated with significant proteinuria and azotemia
90
malignant nephrosclerosis: treatment
aggressive anti hypertensive therapy
dialysis
91
malignant nephrosclerosis: histologic changes
glomeruli: completely fibrotic
arteriole has "onion skin appearance" - thickening of the arterial wall is associated with a hyperplastic arteriosclerosis
92
Leading cause of kidney failure
diabetes (T1 or T2)
93
Diabetic nephropathy: main treatment once proteinuria is diagnosed
Keep BP <130/80
Most effective TX: ACE inhibitors or ARBs
94
Diabetic nephropathy: histological changes
```
glomerulosclerosis
tubulointerstitial fibrosis
arteriolar sclerosis (thick wall and narrow lumen)
```
95
Adult polycystic kidney disease: heredity, population, and description
caused by AUTOSOMAL DOMINANT mutations in PKD 1-3 genes
usually non symptomatic until 3rd or 4th decade
96
Adults polycystic kidney disease: manifestations
drop in kidney function --> CRF
significant HTN - 90% of deaths occur by CV events
97
Adult polycystic kidney disease: description
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
Autosomal recessive polycystic kidney disease: heredity and population
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
autosomal recessive polycystic kidney disease: manifestions
HTN and decrease in urine concentrating ability is one of the most common early manifestations
high levels of Epo
100
PKD: treatment
potential dialysis and then kidney transplant
101
nephrolithiasis: defined
kidney stone found INSIDE kidney
102
urolithiasis: defined
kidney stone that has exited the kidney and is now in the urinary tract
103
Kidney stones are more common in men or women?
men
104
hydronephrosis: common causes
stones in the renal pelvis
| cancers fo the bladder, cervix, uterus, prostate, or other pelvic organs
105
Most common renal neoplasm seen in adults
clear cell carcinoma
106
Explain the name clear cell carcinoma
tubular cells accumulate glycogen and lipids, their cytoplasm appear "clear", lipid laden
107
clear cell carcinoma: manifestations
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
Wilms tumor: population
occurs in children, usually under age 5
109
Wilms tumor: etiology
tumor usually arises as a result of failure of blastemal tissue to differentiate into normal renal structures
110
Wilms tumor: manifestations
at the time of detection, wilms tumors are usually large
presents with pain due to size, fever, high BP, constipation
111
Wilms tumor: TX
neoplasm is aggressive and metastasizes widely, but is responsive to surgery and chemotherapy.
