PREDISPOSING FACTORS PRECIPITATING FACTORS

- glomerulonephritis - chronic strep throat

- strep - post streptococcal
- hepatitis B glomerulonephritis
- chronic kidney disease
(CKD)

Bacterial exposure to Streptococcus a.

Bacterial invasion of mucosa

Bacterial adherence to pharyngeal cells

Inflammation sets in

Release of inflammatory mediators such as cytokines and prostaglandins

Mucosal irritation

Increasing release of local toxins and proteases

Streptococcal pyrogenes and superantigen released

Acts as superantigen stimulating T-cell production Stimulation of agranulocytes release

 Cytokine release Hypothalamic temperature TNF at release
control is stimulated

Endothelial damage and injury

Hemolysis

Vasodilation and edema formation

Leukocyte adhesion to epithelium through expression of adhesion of adhesion molecule

WBC infiltration

Histamine, bradykinins, leukotrienes release

Lymphatic vessels undergo pronounced enlargement in inflamed tissue causing ______ and decreased functionality

PHARYNGITIS (STREP THROAT)

GROUP A STREPTOCCOCAL INFECTION

Pharyngitis left untreated and continually recur (24 x a year for 5 years); proper medication and management adherence

Strep bacteria travel to the kidney and make filtering units (glomeruli) inflamed

Immune complex formation and deposited in glomerular basement membrane

 Complement system is activated to fight pathogens

ACUTE POSTSTREPTOCOCCAL GLOMERULONEPHRITIS

Immune injuries

Cellular proliferation Glomerular basement membrane ___

Capillary lumen narrowed Hematuria; proteinuria

Glomerular blood flow decreased Exposure to infected fluids with Hep. B virus

GFR Virus enter through break of the or mucous membrane

or by injection site into the bloodstream

Oliguria Distal sodium reabsorption Virus reaches liver cells, multiplies and releases
viruses into blood

Sodium and water retention

As hepatocytes are attacked and infiltrated by HBV,
they appear groundglass because HBS Ag
Blood volume infiltrates cells’ cytoplasm

Hypertension and edema set in HEPATITIS B

Recurring for 2 years with hospitalization Immunocomplexes form

 Deposited in the glomeruli of the kidney

CHRONIC GLOMERULONEPHRITIS
Exacerbate glomerulonephritis

Disease progression is not halted with therapeutic management

Progressive damage caused by chronic glomerulonephritis

reduce the kidneys’ ability to filter blood properly
Further causes hepatocyte destruction and scarring of liver

GFR at ≥ 90 mL/min with UO ____

STAGE 1 KIDNEY DISEASE Liver fibrosis sets in

Decreased functional and physical damage is probable; Obstructed portal circulation

GFR: 60-89 mL/min with UO _____
STAGE 2: MILD CHRONIC KIDNEY DISEASE
Portal HTN s/t deposition
of hepatic cellular matrix
Waste product start to build up causing uremia with onset of anemia and HTN

Exacerbate worsening of GFR to 30-59 mL/min with UO _______

STAGE 3: MODERATE CHRONIC KIDNEY DISEASE

Progressive uremia where dialysis is necessary;

GFR: 15-29 mL/min with UO _____
STAGE 4: SEVERE CHRONIC KIDNEY DISEASE Hydrostatic pressure

UREMIA Blood backs up to spleen

Impaired vit. D Phosphate excretion impaired Suppression of RBC Epoetin production

Conversion of inactive D-25 Phosphate levels RBC (short lifespan) RBC and Hgb SPLENOMEGALY
hydroxycholecalciferol to & HEMOLYSIS
1,25 dihydroxycholecalciferol

Vitamin D Serum calcium levels O2 carry C-P Exacerbating

anemia

Intestinal calcium absorption

ANEMIA

Stimulate PTH release

Calcium reabsorption from bone PTH levels

Calcium in bone Renal failure causes

compensatory mechanisms in
calcium and phosphorus

Demineralization of
bone matrix
Secondary hyperparathyroidism

Calcification

Bone becomes fragile

 UREMIA (cont.)

Fluid accumulation Retention of sodium chloride; Uremic toxins Ammonia in GIT Urea in infection
renin

Intravascular volume Altered RAAS Uremic fetor Ammonia breath Ammonia concentration

Cardiac workload Angiotensin II

Vasoconstriction Splanchnic arterial vasodilation

HTN Circulatory blood volume

Left ventricular hypertrophy

RAAS activated

Heart failure
Sodium and water retention

Excess fluid shift from IVS to ISS Backflow of fluid and uremic toxins

Systemic edema Accumulation of toxins in bronchioles

Pressure in hepatic veins and PULMONARY EDEMA
in veins draining to peritoneum

ASCITES

UREMIA (cont.)

Inability to Urea crystals Phosphate levels and Size of sweat glands;

excrete urobilin in the skin crystals in the skin activity of oil glands

Gray-bronze skin Uremic frost Pruritus

Perspiration

Dry ski

UREMIA (cont.)

Platelet function impairment Failure to excrete K+ Allerid (idk)

Abnormal clotting activity K+ accumulation Buffering mechanisms

of kidneys
Bleeding tendencies Hyperkalemia Bicarbonate

Accumulation of
Hydrogen ions

K+ diffuses out

UREMIA (cont.)

Uremic toxin presence of FV overload Atrophy and demyelination of nerve fibers

Pericardium is affected Neuropathy

Inflammation and fibrin formation Peripheral nerve involvement

Fibrin accumulation Motor and sensory nerve conduction

Pericardium surfaces coated Restless

with fibrous exudate leg syndrome
 Vascular collagen tissue deposition Burning
feet syndrome

Fibrous pericardium encases the heart

Pericarditis