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Pathophysiology of Chronic Renal Polycystic Kidney Dse. HPN Nephrosclerosis Systemic Lupus Erythematosus
Intracellular Glucose
Failure Multiple Bilateral Cysts Long Standing HPN Production of large variety of
Non-modifiable Risk Factors: Modifiable Risk Factors: leads to further auto antibodies against normal
Age Diet arteriosclerosis body components such as nucleic
Repeated Inflammation Gender Sedentary Lifestyle acids, RBC, platelet, and WBC
Supports the formation of Heredity Nephrotoxins As cysts fill, enlarge
abnormal glycoprotein in the & multiply, kidneys
basement membrane of also enlarge SLE antibodies react with
glomerulus Ischaemia, Nephron loss, Renal Blood their corresponding antigen
Shrinkage of Kidney
Renal blood vessels &
Stage Renal Reserve nephrons are compressed &
obstructed & functional tse. Forms Immune Complexes
Glomerulosclerosis impairs are destroyed
the filtering fxn. of the Damage to Nephrons
glomerulus thus protein
lost in urine GFR 50% Renal Parenchyma Deposited in the
50% damage Normal BUN, atrophies & become connective tse. such as
Creatinine fibrotic & scarred blood volume & kidneys
80-90% damage
GFR 10-20%
Sharp
Stage Renal Failure BUN,
Na & H2O K+
HCO3 H +
Nitrogenous Erythropoietin Mg +
Vit. D Phosphate Toxins Toxins impair Salivary Deposit of Toxins affect the Toxins causes Retentio
retention retention production retention waste production retention activation retention Continuous decline in renal fxn. irritate WBCs, humoral & urea urea on nerve fibers CNS affectation n of
in kidney impairs pericardial cell mediated breakdown skin
platelets sac immunity;
Hyperkalemia Hyper- Hyperphosphatemi > 90% kidney Fever is Atrophy & Uremic Cells become
Urine magnesemia suppressed; Uremic Uremic Demyalination Encephalopathy resistant to
Output Blood Metabolic GI Bleeding Pericarditi Fetor Frost insulin
Phagocyte becomes
Acidosis stress tendencies Anemia Ca+ Reduction in renal capillaries
defective Peripheral Reduction in
absorption Scarring of Glomeruli
Oliguria Atrophy & Fibrosis of Cardiac Irritation of Neuropathy alertness & Erratic blood
Malfunction Lungs tubules Tamponade Phrenic awareness glucose level
of RAAS Compensates GI Blood loss Hypo- Immune Changes in
bleeding during calcemia System Decline Restless Leg mentation
hemodialysis Stage End Stage Renal Dse. Hiccups Syndrome Because of
Difficulty of
Kussmaul’s (ESRD) glucose
Parathyroid GFR less Risk for Superinfection concentrating
Respiration intracellularly,
overworks than 10% Fatigue
liver produces
Edema Heart Loss of (Hyperpara- Continuous Multisystem Insomnia
tryglycerides
Failure Anorexia appetite thyroidism) Affectation Psychiatric
& HDL
Nausea symptoms
Vomiting
Gastroenteri Fatigue PTH secretion Death
tis Weakne
ss Atherosclerosis
Peptic Ulcer
Pulmonary Edema Ca+ resorption
Peripheral Edema from bone +
Ca absorption
from GI tract Thrombus
& Embolus
Formation
Renal Osteodysthrophy