Pathology Of Renal System

Front 1

Developmental anomalies (renal system)

Back 1

▫Aplasia

▫Hypoplasia

▫Cyst in kidney

Front 2

Single or multiple cysts in pig and dog kidney are reported with what color?

Back 2

yellow color

Front 3

The cysts may arise from ______ due to its distension.

Back 3

nephron

Front 4

Presence of multiple cysts is also termed as _________.

Back 4

congenital polycystic kidney

Front 5

Categories of cysts in the kidney

Back 5

▫Category I (simple cysts)

▫Category II (Mildly complicated benign cysts)

▫Category IIF

▫Category III

▫Category IV (cystic neoplasms)

Front 6

A benign, simple cyst with very thin wall, and does not contain septa, calcifications, or solid material.

Back 6

Category I (simple cysts)

Front 7

The cyst has a density similar to that of water and it does not become enhanced after contrast dye is injected.

Back 7

Category I (simple cysts)

Front 8

A benign cyst that contains a few thin septa, and fine calcifications exist in the wall or septa.

Back 8

Category II (Mildly complicated benign cysts)

Front 9

Also includes uniformly attenuated (whiter than water on CT) lesions less than 3 cm that have sharp edges and do not enhance with contrast dye (do not have their own vasculature).

Back 9

Category II (Mildly complicated benign cysts)

Front 10

Well-defined cyst with sharp edges and multiple septa that may or may not show thickening or enhancement when contrast is given.

Back 10

Category IIF

Front 11

In this category of kidnry cysts, there are no enhancing soft tissue components, and calcifications may be thick and nodular.

Back 11

Category IIF

Front 12

This kidney cysts category also includes uniformly attenuated (whiter than water on CT) lesions greater than 3 cm that have sharp edges and do not enhance with contrast dye.

Back 12

Category IIF

Front 13

An indeterminate cystic mass with thickened, irregular walls and septa that enhance when contrast is given.

Back 13

Category III

Front 14

Malignant cystic masses that have all the characteristics of category III as well as soft tissue components that enhance when contrast is given.

Back 14

Category IV (cystic neoplasms)

Front 15

Functional disturbances in the renal system

Back 15

▫ Proteinuria

▫ Hematuria

▫ Hemoglobinuria

▫ Anuria

▫ Polyuria

▫ Uremia

▫ Glycosuria

▫ Pyuria

▫ Ketonuria

▫ Oliguria

Front 16

Presence of protein particularly albumin in urine.

Back 16

Proteinuria

Front 17

Protein is found as smooth, homogenous, pink staining precipitate also called as ________.

Back 17

Cast

Front 18

TRUE OR FALSE. The presence of albumin in urine is indicative of damage in glomeruli.

Back 18

True

Front 19

It is also characterized by edema due to protein deficiency.

Back 19

Proteinuria

Front 20

Classification of proteinuria

Back 20

▫Overflow proteinuria

▫Tubular proteinuria

▫Glomerular proteinuria

⚬ Transient proteinuria

⚬ Orthostatic proteinuria

Front 21

A result of tubulointersitial disease affecting the proximal renal tubules and interstitium.

Back 21

Tubular proteinuria

Front 22

This results in decreased proximal reabsorption of proteins—in particular, low molecular weight proteins (generally below 25,000 Daltons) such as beta-2 microglobulin

Back 22

Tubular proteinemia

Front 23

Causes of tubular proteinuria

Back 23

o Acute interstitial nephritis

o Immunosuppressive agents

o Analgesics

o Cryoglobulinemia

Front 24

It is most commonly associated with increased production of abnormal low molecular weight proteins (eg, light chains in multiple myeloma, myoglobin in rhabdomyolysis) that exceeds the reabsorption capacity of the proximal tubule, leading to spilling of the protein into the urine.

Back 24

Overflow proteinuria

Front 25

This low molecular protein deposition can induce a glomerulopathy leading to the additional loss of albumin and more profound proteinuria.

Back 25

paraprotein

Front 26

_____ associated with pathological damage to the glomerulus is categorized by protein quantity

Back 26

Glomerular proteinemia

Front 27

TRUE OR FALSE. The more severe the proteinuria, the more significant the glomerular disease.

Back 27

True

Front 28

Primary protein lost in glomerular proteinuria

Back 28

Albumin

Front 29

Types of glomerular proteinemia.

Back 29

✔transient proteinuria

✔orthostatic proteinuria

Front 30

This type of glomerular proteinuria occurs in patients with normal renal function, bland urine sediment, and normal blood pressure.

Back 30

Transient proteinuria

Front 31

The quantitative protein excretion is _____.

Back 31

less than 1 g/day

Front 32

TRUE OR FALSE. Exercise-induced proteinuria usually resolved within 24 hours.

Back 32

True

Front 33

Other term for orthostatic proteinuria

Back 33

postural proteinuria

Front 34

It is characterized by an elevated protein excretion while in the upright position and normal protein excretion in a supine or recumbent position.

Back 34

Orthostatic proteinuria

Front 35

It is characterized by an elevated protein excretion while in the upright position and normal protein excretion in a supine or recumbent position.

Back 35

Orthostatic proteinuria

Front 36

This type of proteinuria is diagnosed if the patient has no proteinuria in early morning samples but has low-grade proteinuria at the end of the day.

Back 36

Orthostatic proteinuria

Front 37

TRUE OR FALSE. The cause of orthostatic proteinuria is not clear but may often relate to obstruction of the left renal vein in the fork between the aorta and the superior mesenteric artery

Back 37

True

Front 38

There is a presence of blood in urine, giving bright red colour.

Back 38

Hematuria

Front 39

It may occur due to damage in glomeruli, tubule or hemorrhage anywhere from glomeruli to urethra.

Back 39

Hematuria

Front 40

Common causes of hematuria

Back 40

o UTI

o Kidney infections (pyelonephritis)

o Bladder and Kidney stones

Front 41

When hemoglobin is present in urine without erythrocytes due to intravascular haemolysis.

Back 41

Hemoglobinuria

Front 42

Color of urine in hemoglobinuria.

Back 42

Brownish red

Front 43

Etiology of hemoglobinuria

Back 43

Caused by various infections such as:

o Leptospira spp.

o Babesia spp.

o Phosphorus deficiency

Front 44

Difference in urine color b/w hematuria and hemoglobinuria after centrifugation.

Back 44

✔ Hematuria- clear yellow urine supernatant.

✔ Hemoglobinuria- clear red

Front 45

Etiology of Anuria

Back 45

o Absence of urinary secretion due to glomerulonephritis o Inelastic renal capsule unable to exert sufficient pressure required for glomerular filtration leading to nephrosis.

o Due to hydronephrosis or calculi, urine already secreted puts back pressure to prevent further secretion.

o Low blood pressure

o Dehydration

o Necrosis of tubular epithelium

Front 46

Absence of urine

Back 46

Anuria

Front 47

Increased amount of urine leading to frequent urination due to diabetes insipidus, hormonal imbalance and polydipsia.

Back 47

Polyuria

Front 48

TRUE OR FALSE. In polyuria, waste products are successfully eliminated.

Back 48

True

Front 49

Types of Diabetes Insipidus

Back 49

✔ Central (cranial) diabetes insipidus

✔ Nephrogenic diabetes insipidus

✔ Gestational diabetes insipidus

✔ Dipsogenic diabetes insipidus or psychogenic polydipsia

Front 50

In this type of diabetes insipidus, the production or release of ADH is too low to stop the kidneys from passing dilute urine.

Back 50

Central (cranial) diabetes insipidus

Front 51

Central diabetes insipidus results in:

Back 51

o increased loss of water

o more thirst.

Front 52

Etiology of central diabetes insipidus

Back 52

✔Genetic inheritance of a mutation in the vasopressin gene, AVP-NPII.

✔Brain tumors such as pituitary adenoma and craniopharyngiomas

✔Head injury causing damage to the pituitary gland or hypothalamus.

✔Injury may also result after brain surgery.

✔Blood vessel complications such as those during pregnancy where the blood supply to the hypothalamus and pituitary gland may be compromised.

✔Stroke or sudden loss of oxygen to the brain (e.g. during anesthesia or drowning) may also result in diabetes insipidus.

Front 53

Vasopressin gene affected by mutation in central diabetes insipidus

Back 53

AVP-NPII

Hint 53

The pattern of inheritance is autosomal.

Front 54

Conditions that may also affect the pituitary gland and the hypothalamus.

Back 54

✔Meningitis

✔Encephalitis

✔Brain infections

Front 55

This type of diabetes insipidus have adequate amounts of ADH in the body but the kidneys fail to respond it.

Back 55

Nephrogenic diabetes insipidus

Hint 55

the urine is not concentrated

Front 56

Etiology of nephrogenic diabetes insipidus

Back 56

✔ Familial or genetic causes resulting from mutation in the AQP2 gene that codes for aquaporin-2 protein.

✔ Autosomal recessive pattern of inheritance

✔ Metabolic causes such as high blood sugar, high blood calcium and low potassium.

✔ The use of drugs such as lithium used to treat bipolar disorder can decrease the expression of aquaporin-2.

✔ Diseases such as amyloidosis, obstructive uropathy, chronic kidney disease and polycystic kidney disease.

Front 57

Mutation in this gene is one of the etiology of nephrogenic diabetes insipidus

Back 57

AQP2 gene or aquaporin-2 gene

Front 58

Metabolic disorders that may cause nephrogenic diabetes insipidus.

Back 58

high blood sugar, high blood calcium and low potassium.

Front 59

This drug is used to treat bipolar disorder, which can decrease the expression of aquaporin-2.

Back 59

lithium

Front 60

Diseases that may cause nephorgenic diabetes insipidus.

Back 60

▫amyloidosis

▫obstructive uropathy

▫chronic kidney disease

▫polycystic kidney disease.

Front 61

This type of diabetes insipidus are and occurs only during pregnancy.

Back 61

Gestational diabetes insipidus

Front 62

This type of DI sually develops in the third trimester and remitting spontaneously 4-6 weeks post-partum.

Back 62

Gestational diabetes insipidus

Front 63

Main cause of gestational diabetes insipidus

Back 63

excessive vasopressinase activity

Front 64

It is an enzyme expressed by placental trophoblasts which metabolises arginine vasopressin (AVP)

Back 64

Vasopressinase

Front 65

TRUE OR FALSE. Activity is proportional to the placental weight

Back 65

True

Hint 65

higher vasopressinase activity in third trimester or in multiple pregnancies.

Front 66

Vasopressinase is metabolised by the _____.

Back 66

Liver

Front 67

TRUE OR FALSE. Vasopressinase is at higher concentrations in pregnant women with hepatic dysfunction, such acute fatty liver of pregnancy, hepatitis and cirrhosis.

Back 67

True

Front 68

It is also known as dipsogenic diabetes insipidus or psychogenic polydipsia.

Back 68

Primary polydipsia

Front 69

This type of diabetes insipidus can cause excretion of large volumes of diluted urine.

Back 69

Primary polydipsia

Front 70

The underlying cause of primary polydipsia is _____.

Back 70

intake of excessive fluids

Hint 70

Prolonged excessive water intake by itself can damage the kidneys and suppress ADH

Front 71

Can be the result of abnormal thirst caused by damage to the thirst-regulating mechanism, situated in the hypothalamus.

Back 71

Primary polydipsia

Front 72

The presence of harmful waste products like uric acid, creatinine and urea in blood due to damage in kidneys or obstruction by inflammation, neoplasm, abscess and presence of calculi.

Back 72

Uremia

Front 73

Cause of uremia.

Back 73

Urine that remains in the system

Front 74

This condition is characterized by headache, vomiting, hyperirritability, convulsion, ulcers in oral cavity and stomach, normochromic and normocytic anemia, hemosiderosis and thrombocytopenia.

Back 74

Uremia

Front 75

There is irritation of the tissues from the ammonia produced by the bacterial degradation of urea.

Back 75

Oral Ulceration or Uremic Stomatitis

Hint 75

In severe cases, there may be extensive subepithelial necrosis and sloughing of the tip of the tongue.

Front 76

Uraemic vasculitis and thrombosis lead to ________.

Back 76

necrosis and sloughing of the mucosa.

Hint 76

The lesions are often very painful and contribute to the anorexia often observed in animals with chronic kidney disease.

Front 77

Pathophysiology of gastric ulceration

Back 77

Front 78

Pathophysiology of gastric ulceration

Back 78

Front 79

Pathophysiology of uremic encephalopathy

Back 79

Front 80

Clinical factors or diseases that may cause anema.

Back 80

o Iron deficiency

o Vitamin deficiencies (eg, folate, vitamin B-12)

o Hyperparathyroidism

o Hypothyroidism

o Decreased red blood cell survival

Front 81

A hormone necessary for RBC production in bone marrow.

Back 81

Erythropoietin

Front 82

Erythropoietin is produced by ________ in the kidney in response to hypoxia.

Back 82

peritubular cells

Front 83

Elevated PTH levels are thought to be associated with ______, which may suppress RBC production and lead to a hypoproliferative anemia.

Back 83

marrow calcification

Front 84

An acute phase protein involved with iron metabolism, plays a key role in erythropoiesis.

Back 84

hepcidin

Front 85

TRUE OR FALSE. Hepcidin, up-regulated in states of inflammation, prevents iron absorption in the small intestine, as well as iron release from macrophages

Back 85

True

Front 86

Presence of glucose in urine.

Back 86

Glycosuria

Hint 86

It may occur due to insulin deficiency – diabetes mellitus

Front 87

Glycosuria may occur in sheep due to enterotoxaemia caused by _________.

Back 87

Clostridium perfringens type D

Front 88

Pathophysiology of enterotoxemia

Back 88

Front 89

Presence of pus in urine due to suppurative inflammation in urinary tract.

Back 89

Pyuria

Front 90

There is decreased amount of urine which occurs due to glomerulonephritis, obstruction in urinary passage, dehydration, low blood pressure and tubular damage.

Back 90

Oliguria

Front 91

It is the degeneration and necrosis of tubular epithelium without producing inflammatory reaction.

Back 91

Nephrosis

Hint 91

It mostly includes acute tubular necrosis as a result of ischemia or toxic injury to kidney.

Front 92

It is characterized by necrosis and sloughing of tubular epithelial cells exhibited by uremia, oliguria, anuria

Back 92

Nephrosis

Front 93

Etiology of nephrosis

Back 93

o Hypotension

o Heavy metals

o Mycotoxins e.g. Ochratoxin

o Antibiotics e.g. Gentamicin

Front 94

Macroscopic features of nephrosis.

Back 94

o Swelling of kidneys.

o Capsular surface smooth, pale and translucent.

Front 95

Microscopic features of nephrosis.

Back 95

o Vacuolation in tubular epithelium.

o Coagulative necrosis

o Sloughing of tubular epithelium

Front 96

Two current hypotheses for the formation of edema in nephrotic syndrome.

Back 96

◾The underfill hypothesis holds that the loss of albumin leading to lower plasma colloid pressure is the cause.

◾The overfill hypothesis states that the edema is due to primary renal sodium retention.

Front 97

Pathophysiology of underfill hypothesis

Back 97

Front 98

An intrinsic defect in the renal tubules which cause a decrease in sodium excretion.

Back 98

Overfill hypothesis

Hint 98

This could occur if the filtered intraluminal protein directly stimulates renal epithelial sodium reabsorption.

Front 99

Two facts support overfill hypothesis:

Back 99

✔ sodium retention is observed even before the serum albumin level starts falling

✔ intravascular volume is normal or even increased in most patients with nephrotic syndrome

Front 100

Inflammation of glomerulus

Back 100

Glomerulonephritis

Front 101

Inflammation of glomeruli primarily characterized by:

Back 101

✔ pale and enlarged kidneys with potential haemorrhage

✔edema of glomeruli

✔congestion

✔infiltration of inflammatory cells

Front 102

Due to presence of mesangial proliferation, it is also called ________

Back 102

mesangio-proliferative glomerulonephritis (MPGN)

Front 103

Etiology of glomerulonephritis

Back 103

o Streptococci infection

o Immune complexes

o Environmental pollutants such as Organochlorine pesticides

Front 104

Pathophysiology of Lupus nephritis

Back 104

Front 105

Macroscopic features of glomerulonephritis

Back 105

o Enlarged kidneys

o Edema, pale kidneys

o Petechiae on kidneys

o Proteinuria, uremia, hypercholesterolemia and increased creatinine level in blood.

Front 106

Microscopic features of glomerulonephritis

Back 106

o Edema of glomeruli leading to increase in size.

o Infiltration of neutrophils, macrophages.

o Compression of blood capillaries and absence of erythrocytes.

o Thrombosis and necrosis of glomerular capillaries.

Front 107

Types of glomerulonephritis

Back 107

▫Type-I MPGN

▫Type-Il MPGN (Membranous)

▫Type III MPGN (Acute Proliferative)

▫Chronic glomerulonephritis

▫Focal embolic glomerulonephritis

Front 108

⚬Proliferation of mesangial cells, and there is deposition of immune complexes containing IgG, IgM, IgA and C3;

⚬Proliferation and swelling of endothelial cells.

Back 108

Type-I MPGN

Hint 108

Immune complexes penetrate vascular endothelium but not the basement membrane and are deposited in subendothelial region.

Front 109

Immune complexes induce production of _________ which increases production of fibrinolectin, collagen and proteoglycans leading to thickness of basement membrane.

Back 109

transforming growth factor (TGFB1)

Front 110

increase in production of fibrinolectin, collagen and proteoglycans leads to thickness of basement membrane.

Back 110

Wireloop lesion

Front 111

Deposition of immune complexes in basement membrane (lamina densa) due to uncontrolled activation of complement.

Back 111

Type-Il MPGN (Membranous)

Front 112

Proliferation of endothelium and mesangial cells, & demonstration of C3 component, no immunoglobulin.

Back 112

Type-Il MPGN (Membranous)

Front 113

Subepithelial deposits of immune complexes and disruption of basement membrane.

Back 113

Type III MPGN (Acute Proliferative)

Hint 113

✔Demonstration of IgG in subepithelial region.

✔Congestion and oedema of glomeruli.

✔Infiltration of neutrophils, macrophages and lymphocytes.

Front 114

Swelling of epithelium and its proliferation forming ________.

Back 114

"Epithelial cresent"

Front 115

Proliferation of epithelial and endothelial cells.

Back 115

Chronic glomerulonephritis

Hint 115

Reduplication, thickening and disorganization of glomerular basement membrane.

Front 116

Entire glomerulus is replaced by Hyaline connective tissue.

Back 116

Chronic glomerulonephritis

Hint 116

Lumen of capillaries occluded

Front 117

Focal zone of necrosis in glomeruli.

Back 117

Focal embolic glomerulonephritis

Front 118

Proliferation of epithelial cells and formation of crescent.

Back 118

Focal embolic glomerulonephritis

Hint 118

Infiltration of neutrophils

Front 119

Inflammation of kidney characterized by degeneration and necrosis of tubular epithelium, edema and infiltration of inflammatory cells in interstitium.

Back 119

Interstitial nephritis

Front 120

Etiology of interstitial nephritis

Back 120

 Ochratoxins

 Leptospira

 Toxins/ poisons e.g. pesticides.

 Herpes virus

 Endogenous toxaemia e.g. ketosis  Immune complexes

Front 121

Macroscopic features of interstitial nephritis

Back 121

o Enlargement of kidneys

o Necrosis, congestion and haemorrhage

Front 122

Microscopic features of interstitial nephritis

Back 122

✔ Oedema, congestion, haemorrhage.

✔ Necrosis and degeneration of tubular epithelium.

✔ Infiltration of inflammatory cells like neutrophils, macrophages and lymphocytes in interstitium.

✔ Loss of tubules, foci of mononuclear cells, fibrosis in chronic cases.

✔ Immune complexes are deposited in granular form causing degeneration of epithelial cells of tubules and mononuclear cell infiltration.

Front 123

Inflammation of renal pelvis and parenchyma (i.e. tubules) characterized by congestion, suppurative inflammation and fibrosis.

Back 123

Pyelonephritis

Front 124

Etiology of pyelonephritis

Back 124

o Corynebacterium renale

o Staphylococcus aureus

o E. coli

o Actinomyces pyogenes

o Pseudomonas aeruginosa

Front 125

Macroscopic features of pyelonephritis

Back 125

 Congestion, haemorrhage and abscess formation in renal cortex, pelvis and ureters