Path II-Nephritic Syndrome (2/2glomerulonephritis)

Question 1

Describe Nephritic syndrome

Answer 1

In Nephritic syndrome, an unknown agent damages the glomerulus.

There is increase in permeability to proteins and RBC from the blood but paradoxically, there is decreased permeability to water.

The decrease in permeability to water leads to Oliguria.

Question 2

Clinical manifestation of nephritic syndrome:

Hematuria(w/ RBC casts)

Answer 2

Blood in urine due to increased permeability of glomerular wall.

Cast are rod shaped proteins found in urine that are surrounded by RBC in hematuria.

Question 3

Clinical manifestation of nephritic syndrome:

Oliguria

Answer 3

2/2 decreased permeability of water

Decreased urine

Question 4

Clinical manifestation of nephritic syndrome:

What is the normal amount of diuresis vs the amount with Nephritic syndrome?

Answer 4

Normal 1.3-1.6L (24hr)

Nephritic Syndrome: <400mL

Question 5

Clinical manifestation of nephritic syndrome:

Why does the concentration of waste metabolites increase in the blood with Oliguria?

Answer 5

The increase in due to the fact that water, as well as waste products can’t be deposited into urine so the metabolites from the body continue to accumulate in the body.

I.e. Nitrogen

Question 6

Clinical manifestation of nephritic syndrome:

Term for nitrogen containing waste products in blood

Answer 6

Azotemia

Recall nitrogen AKA Azod

Question 7

Clinical manifestation of nephritic syndrome:

Oliguria leads to Azotemia, explain azotemia.

Answer 7

Increase of nitrogen in blood slowly; eventually pt gets sick.

Not felt by patient.

Question 8

Clinical manifestation of nephritic syndrome:

What is the definition of azotemia?

Answer 8

A biochemical abnormality that refers to an elevation of blood urea nitrogen and creatinine levels and is largely related to a decreased glomerular filtration rate.

Question 9

Clinical manifestation of nephritic syndrome:

How to dx azotemia?

Answer 9

Biochemical test

Blood test

Question 10

Clinical manifestation of nephritic syndrome:

Azotemia + combination of signs and symptoms =

Answer 10

Uremia

Recall that this is felt by the patient

Question 11

Clinical manifestation of nephritic syndrome:

Explain the dynamics of filtration

Answer 11

Filtration is based on arterial hydrostatic blood pressure.

This hydrostatic pressure must be greater than 50mmHg due to meeting resistance.

Resistance is due to the accumulation of urine in the bowman capsule(18mmHg) and Glomerular colloid osmotic pressure (32mmHg due to proteins).

Question 12

Clinical manifestation of nephritic syndrome:

How does a a drop arterial hydrostatic pressure lead to hypertension ?

Answer 12

Normally: decreased Arterial BP —> filtration stops —>renin secreted by juxtaglomeruli cells —> angiotensin II (strongest vasoconstrictor in body) —> increased BP —> increased filtration .

Glomerulonephritis: Damage to glomeruli wall —> decreased filtration —> juxtaglomeruli release renin —> angiotensin II —> increased BP —> no increase in filtration (damage to wall not true drop in arterial hydrostatic pressure)

Question 13

Clinical manifestation of nephritic syndrome:

What are the two stimulants of renin release?

Answer 13

1. Drop in arterial hydrostatic pressure <50mmHg

2. Decrease glomeruli filtration rate

Question 14

Disorders a/w nephritic syndrome:

Common glomerulonephritis in children in 1st decade of life.

Decrease in defense in mouth —> bacterial overgrowth (streptococcal)—> tonsillitis —> Ab against strep Ag & Glomeruli Ag because of similar appearance —> IC —> phagocytic attraction—> glomerulonephritis

Answer 14

Acute proliferative glomerulonephritis

Question 15

Disorders a/w nephritic syndrome:

What is the bacterial agent of Acute proliferative glomerulonephritis?

Answer 15

Beta-hemolytic strepcoccus group A

Strep Pyogenes

Question 17

Disorders a/w nephritic syndrome:

Term for action of Ab against glumerlus Ag in acute proliferative glomerulonephritis

Answer 17

Molecular mimicry

Question 18

Disorders a/w nephritic syndrome:

Is Acute proliferative glomerulonephritis simply due to infection?

Answer 18

No, although it is an infectious disease it is also due to the confusion of Abs, that attack the glomeruli Ags as well.

Question 19

Disorders a/w nephritic syndrome:

What are the characteristics of APG?

Answer 19

1. Hematuria w/ casts
2. Oliguria
3. Azotemia
4. Hypertension
5. Possibly swelling (swelling always in nephrotic syndromes not always nephritic)

Question 20

Important note from Dr. B, if swelling is noticed under the eyes of children within 1st decade of life, what must be done?

Answer 20

Kidney exams as it could indicate kidney pathology

Question 21

Disorders a/w nephritic syndrome:

Define streptolysin O

Answer 21

Hemolytic exotoxins made by streptococcus

“O” because oxygen liabile

Question 22

Disorders a/w nephritic syndrome:

What other disorders is streptolysin seen in?

Answer 22

Rheumatic fever

Question 23

Disorders a/w nephritic syndrome:

Tx and recovery rate of adults and children with acute proliferative glomerulonephritis?

Answer 23

Tx= corticosteroid- much catch disease in early stage

Children=99% recovery

Adults= 50% recovery & 50% develop chronic APG

Question 24

Disorders a/w nephritic syndrome:

Disease characterized bu rapid progressive loss of renal function a/w severe Oliguria and if untreated, death within weeks to months from renal failure.

Secondary disease of the kidney (usually associated w/ immunopathology

Answer 24

Rapidly progressive -Crescentic- Glomerulonephritis

Question 25

Disorders a/w nephritic syndrome:

Why is Rapidly progressive glomerulonephritis referred to as crescentic?

Answer 25

Hyperplasia of parietal epithelial cells of the Bowman’s capsule occludes efferent arterioles.

Crescent shaped formed occluding proximal convoluted tubules, increasing intracapsular hydrostatic pressure leading to pressure atrophy of glomerular

Question 26

Disorders a/w nephritic syndrome:

Describe type 1 rapidly progressive glomerulonephritis

Answer 26

1. Called Anti-GBM if glomeruli, and antiABM if alveoli
2. A/w type 2 (Ab dependent) hypersensitivity rxn
3. 50% idiopathic
4. Dx with Bx. Looking for presence of crescents. High crescent more fatal
5. A/w Goodpasture syndrome

Question 27

Disorders a/w nephritic syndrome:

Describe Goodpasture syndrome in association with type I RPGN

Answer 27

Goodpasture is developed as a result of Ab against the basement membrane of the lungs and kidney.

Question 28

Disorders a/w nephritic syndrome:

Lung involvement in Goodpasture syndrome

Answer 28

Anti-GBM Abs enter the alveoli due to an insult of the capilaries.

The Ab bind to Ag and causes complement cascade leading to destruction of alveoli.

Pt experience coughing of bloody sputum (Hemoptysis)

Pneumonitis

Question 29

Disorders a/w nephritic syndrome:

Glomeruli involvement in Goodpasture syndrome

Answer 29

Glomerulonephritis

Presence of crescencies

Question 30

Disorders a/w nephritic syndrome:

Tx for type 1 RPGN

Answer 30

1. Plasmapharesis: results in full recovery. Removal of blood through vein or artery. Centrifuged, then removal of plasma which contains lots of Ab and then blood placed back into body
2. Corticosteroids
3. Immunosuppressants

Question 31

Disorders a/w nephritic syndrome:

Plasmapharesis can also be helped in which diseases

Answer 31

Systemic Lupus Erythmatous

Question 32

Disorders a/w nephritic syndrome:

How to dx Acute proliferative glomerulonephritis?

Answer 32

1. Low serum complement level (hypocomplementemia) a/w Immune complex type hypersensitivity rxn.
2. Elevation of serum anti-streptolysin O tigers