Lecture 1 Flashcards

(53 cards)

1
Q

What are the functions of the kidneys

A

1) Regulation of water and electrolyte content
2) retention of substance vital to the body
3) Martian acid base valence
4) excretion of waste products
5) endocrine functions

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2
Q

What are the steps for urine formation

A

Filtration
Secretion
Reabsorption

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3
Q

What is Azotemia
pre renal and post renal

A

Elevation of blood urea nitrogen and creatine levels and we have a decreased GFR.

Prerenal azotemia is caused (when there is hypoperfusion of the kidneys) so it decreases GFR without parenchymal damage.

Postrenal azotemia is caused when urine flow is obstructed below the level of the kidney, relief of the obstructed is followed by the correction of the azotemia

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4
Q

What is nephritic syndrome

A

Caused by glomerular injury ( inflammation of the glomeruli) we have visible hematuria, proteinuria, azotemia, edema and hypertension it is a presentation is acute post streptococcal glomerulonephritis

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5
Q

What are the types of hematuria

A

Microhematuria: blood is not visible in the urine, detection under microscope, damage to glomeruli, UTIs

Macrohematuria: blood viable in the urine, pink, red dark brown discoloured, large or small blood clots, damage to the kidneys

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6
Q

What is nephritic syndrome

A

Caused by glomerular inflammation which causes GBM damage causing loss of RBCs. Patient will present with low GFR AND:

Think: “PHAROH” mnemonic
Proteinuria
Hematuria
Azotemia
Renal failure
Oliguria
Hypertension

causes are: goodpasture syndrome, Alport syndrome

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7
Q

What is Nephrotic syndrome

A

Podocyte damage causing impaired charge barrier causing proteinuria
Patient presents with massive proteinuria and frothy urine with fatty casts

Examples are: Focal segment glomeruloscleoris and amyloids

causes: idiopathic nephrotic syndrome, glomerulonenepritis ect,

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8
Q

What is nephritic nephrotic syndrome

A

Severe GBM damage loss of RBCs into urine, causes hematuria and proteinuria

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9
Q

What is infection related glomerulonenephritis

A

Type III hypersensitivity reaction

in children we see it after a streptococcal pharyngitis infection

in adults staphylococcus is an additional causative agent.

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10
Q

What is IgA neuropathy ( Berger disease )

A

accumulation of IgA in the mesangium leading to inflammation and damage. so blood leaks into the urine.

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11
Q

What is rapidly progressive (cresentic) glomerulonephiritis

A

we have severe glomerular injury and a loss of renal function, we see servere oliguria. associated with presence of crecents. caused by good pasture syndrome, characterised by P or C ANCA

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12
Q

what is diffuse proliferative glomerulonenephiritis

A

accumulation of IgG and C3

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13
Q

alport syndrome

A

caused by mutation of type 4 collagen, commonly X linked. males are more effected, mutations in other collagen genes (α3 or α4).

we can have hematuria, proteinuria and progression to renal failure.
eye problems and hearing loss

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14
Q

minimal change disease

A

loss of antithrombin, no changes
mainly in children, Selective proteinuria and hypoalbuminemia that occurs in the absence of cellular glomerular infiltrated or immunoglobulin deposits

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15
Q

focal segmental glomerulosclerosis

A
  • a disease where some parts of some glomeruli get scarred, which affects how the kidney filters blood.

. Primary (idiopathic)
Meaning the cause is unknown.
It often starts in juxtamedullary glomeruli (the ones deep in the kidney near the medulla).
2. Secondary (due to another condition):
HIV infection (→ HIV-associated nephropathy)
Heroin abuse (→ heroin nephropathy)
As a result of other glomerular diseases, like IgA nephropathy. complication of sickle cells, obesity or congenital malformation

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16
Q

membraneous neuropathy

A

we have diffuse capillary and GBM thickening seen on the microscope

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17
Q

what is asymptomatic hematuria

A

there are no clinical feature but we can find RBCs in the urine

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18
Q

acute kidney injury

A

we have anuria and onset of azotemia can result from glomerular injury, interstitial injury and vascular injury

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19
Q

chronic kidney disease

A

prolonged symptoms, progressive scarring in the kidney from any cause.

we usually see proteinuria, hypertension or azotemia

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20
Q

UTI

A

bacteriuria and pyuria, it can be asymptomatic or symptomatic

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21
Q

nephroliithiasis

A

renal stones, recurrent stone formation

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22
Q

what is creatine and what is BUN

A

creatine: waste product of muscle and protein metabolism, test measures and assesses kidney function, found in the muscle, serum, plasma and urine

BUN: blood urea nitrogen used to check hydration status, measure urea nitrogen levels in blood, it is effected by the diet and it is found in the blood.

23
Q

what are simple cysts

A

does not communicate with collecting system and mostly asymptomatic and hematuria from cyst rupture

24
Q

autosomal dominant (adult) polycystic kidney disease

A

multiple expanding cysts in both kidneys, one of the causes for chronic kidney disease, can be caused by inheritance of 2 autosomal dominant genes

intermittent gross hematauria usually occurs
kindly may weigh up to 4kg, the cysts are filled with fluids.

25
autosomal recessive (childhood) polycystic kidney disease
rare autosomal recessive disorder, mutations the PKHD1 gene which codes for fibrocystic on short arm of chromosome 6. perinatal and neonatal are the most common patients who survive infancy can develop liver cirrhosis.
26
what are the medullary diseases with cysts
medullary sponge kidney - associated with nephrolithasis associated with renal dysfunction. nephronophthisis: medullary cystic diseasee usually begins in childhood, 9 gene. loci have been identified.
27
hydronephrosis
dilation of the renal pelvis, progressive atrophy of the kidney due to obstruction to the outflow of urine. even if it is completely obstructed the glomerular filtration still presists and reruns to the lymphatic and venous system due to this the renal pelvis dilates.
28
what are the mechanisms of glomerular injury and disease
slide 24
29
glomerular disease pathogenesis
immunologically mediated: - immune complex - Anti GBM - other immune mechanisms non immune: metabolic, vascular and hereditary glomerular injury caused by: complement and neutrophils macrophages complement and membrane attack complex cytotoxic antibodies
30
what are the 2 forms of antibody associated injury
- injury resulting from soluble circulating antigen antibody complex in the glomerulus - injury by antibodies reacting in situ within th glomerulus.
31
what is anti glomerular basement membrane antibody mediated glomerulonephritis ( good pastures syndrome)
autoimmune kidney disease where the body’s immune system makes antibodies that mistakenly attack the glomerular basement membrane (GBM), Specifically, they target a protein in the α3 chain of type IV collagen, which is a structural protein in the GBM. In some people, the same autoantibodies also attack the basement membranes in the lungs (specifically the alveoli). This causes lung bleeding along with kidney damage. This combined condition is called Goodpasture syndrome.
32
what is membranoproliferative glomerulonenephritis
complications with hepatitis B and C characterised by the deposition of the complement system type of chronic glomerulonephritis, meaning it causes long-term inflammation and damage in the glomeruli MPGN Type I: 🧫 Caused by immune complex deposition (antigen-antibody complexes getting stuck in the kidney) Immune deposits found in subendothelial space (between endothelium and GBM) Often associated with other infections or autoimmune diseases (like Hep C, lupus) 🧫 Dense Deposit Disease (DDD) – formerly MPGN Type II: Characterized by dense ribbon-like deposits within the GBM Believed to be caused by abnormal activation of the complement system (part of the immune response) Much rarer and more severe
33
acute post infectious (poststreptococal) glomerulonenephritis
a type of glomerular disease that happens after an infection, usually a few weeks later. It’s caused by the immune system reacting to the infection and accidentally damaging the kidneys. we have an infiltration f neutrophil and leukocytes The body forms immune complexes (antigen-antibody pairs) to fight off an infection. These immune complexes get stuck in the glomeruli, which are tiny filters in the kidneys. triggers are exogenous (outside the body) and endogenous (inside the body) : exo - staphylococcus infections, viral infections e.g chickenpox endo: autoimmune conditions like SLE
34
hereditary nephritis
a group of kidney diseases that are passed down through families. These diseases are caused by mutations in the genes responsible for making glomerular basement membrane (GBM) proteins.Alport Syndrome
35
alport mimic
MYH9 disease which encodes the non muscle myosin heavy chain IIA causes: epstein syndrome fetter syndrome
36
What is Anti-GBM Antibody–Mediated Crescentic Glomerulonephritis
caused by the immune system attacking the glomerular basement membrane (GBM) of the kidneys. Anti-GBM antibodies are autoantibodies that target collagen in the GBM Linear deposition of IgG antibodies along the GBM and linear deposition of C3 these patients are sait to have goof pasture syndrome: Goodpasture Syndrome is a special case of anti-GBM antibody disease. It happens when the anti-GBM antibodies not only attack the kidneys but also target the pulmonary alveolar basement membranes (in the lungs)
37
Immune Complex–Mediated Crescentic Glomerulonephritis
crescentic glomerulonephritis (GN) where immune complexes (antigen-antibody complexes) accumulate in the glomeruli, leading to inflammation and damage to the glomerular basement membrane (Crescents are a complication)
38
Pauci-Immune Crescentic Glomerulonephritis
rapidly progressive glomerulonephritis (RPGN) where the immune system causes crescent-shaped lesions in the kidneys. we have minimal or no detectable immune complexes in the glomeruli. - no anti GBM antibodies - ANCA related symptoms: oliguria and proteinuria and azotemia.
39
Tubulointerstitial Nephritis
a group of inflammatory conditions that primarily affect the interstitium and the tubules, The glomeruli, which are the kidney’s filtration units, may be spared or affected later in the disease. caused by bacterial infection. or it can be drug induced
40
acute tubular injury
Damaged tubular epithelial cells and Rapid decline in kidney function Tubular epithelial cells in the kidneys (which help reabsorb substances from urine) get injured or die. As a result, the kidneys stop filtering properly, and waste builds up in the body. This leads to acute kidney injury (AKI), which is a sudden loss of kidney function.
41
what are some diseased involving blood vessels:
1) Arterionephrosclerosis refers to the hardening and thickening of small arteries and arterioles in the kidneys, typically associated with benign (chronic) hypertension. we also have hyaline arteriosclerosis where the walls of small arteries get thickened. we have benign HTN malignant HTN: blood pressure becomes extremely high, causes rapid organ damage, especially to the kidneys, eyes, brain, and heart. it is greater than 200/120mm Hg, in the kidneys it can lead to fibrinoid necrosis, hyperplasticity arteriosclerosis and acute kidney injury. left ventricular failure may occur too. Thrombotic Microangiopathies (TMAs): widespread formation of tiny blood clots (thrombi) in the smallest blood vessels, causes can be: HUS haemolytic uremic syndrome, various drugs, malignant hypertension.
42
what are some causes for chronic renal failure
pathologic - tumors, transplant rejection, congenital disease and glomerulonephritis physiologic: hypertension, diabetes mellitus, chronic UTIs and hIV
43
yes of kidney failure
acute: sudden loss of kidney function caused by illness, injury or a toxin Chronic: long and slow when the kidneys progressively loose their ability to function end stage: kidneys have completely and permanently shut down
44
5 stages of kidney disease
stage 1: normal or high function stage 2: mildly decreased function stage 3: mild to moderate decreased function stage 4: severly decreed function stage 5: kidney failure
45
what is a consequence of renal failure
MAD HUNGER Metabolic Acidosis Dyslipidemia High potassium High potassium Uremia - high serum urea Na+ retention Growth retardation and developmental issues Erythropoietin deficiency Renal osteodystrophy
46
patient with uremias presents with what
pericarditis, encephalopathy, anorexia and nausea.
47
what is renal osteodystrophy
hypokalcemia, hyperphosphatemia and failure of vitamin D hydroxylation, associated with chronic KD, causes thinning of bones
48
kidney stones
to treat and print we encourage fluid intake. content: - calcium: vitamin C overuse, malabsorption ammonium magnesium phosphate: e.g - ---- - calcium phosphate, caused by infection with grease - uric acid: acidic pH is a risk factor, seen in diseases with increase cell turnover - cystine: hereditary, cystine reabsorbing PCT, ornithine, lysine, arginine ( COLA)
49
pyelonephritis
acute: neutrophils infiltrate renal interstinium, affects cortex, causes can be UTI, we have WBCs in the urine. chronic: recurrent or inadequately treated acute pyelonephritis, predisposition to infections
50
tumors of the kidneys
Oncocytoma: benign tumor, Arises from intercalated cells of the collecting ducts. genetic changes, loss of chromosome 1, 14 and Y. What is Renal Cell Carcinoma: malignant (cancerous) kidney tumor in adults. It originates from the renal tubular epithelium, so it's mainly found in the renal cortex, smoking is the strongest risk factor. and occupational exposure to cadmium. Clear Cell Carcinoma: tumor cells have a “clear” cytoplasm under the microscope, originates from Proximal tubular epithelium, clear appearance is due to accumulated lipids and glycogen, it is associated with VHL (Von-Lindau disease) Caused by mutations in the VHL tumor suppressor gene (on chromosome 3p) Papillary Renal Cell Carcinoma: mutations in the MET proto-oncogene, MET function: It codes for a tyrosine kinase receptor that binds hepatocyte growth factor (HGF) Chromophobe Renal Cell Carcinoma: Arises from intercalated cells of the collecting ducts, Extensive loss of whole chromosomes, Chromosomes lost: 1, 2, 6, 10, 13, 17, and 21
51
von hippel lindau syndrome
autosomal dominant, we have visceral cysts eye tumor brain tumour kidney tumor VHL disease is inherited as an autosomal dominant trait and is characterized by predisposition to a variety of neoplasms, but particularly to hemangioblastomas of the cerebellum and retina.
52
bladder cancer
more common than kidney cancer, we have painless hematuria.
53
horseshoe kidney
inferior poles of kidneys fuse, trapped under inferior mesenteric artery