CFB PBL 3 Flashcards
Describe the anatomy and main functions of the kidney
Anatomy
Retroperitoneal (not in peritoneum)
Enclosed in fibrous capsule
Outer cortex and inner medulla
1 million nephrons
Each nephron has a glomerulus in Bowman’s capsule
It has a proximal tubule, descending and ascending loop of Henle, DCT and CT
Right kidney slightly lower - due to liver
Function
1.Filters waste products from blood
2.Balances electrolytes
3.Maintain fluid balance
4.Producing erythropoietin - for RBC production
5.Produces active form of Vitamin D for Ca 2+ reabsorption
6.Producing Renin - regulating blood pressure
7.Regulating acid base homeostasis
Explain the importance of GFR (Glomerular filtration rate) in assesing renal function and staging of chronic renal failure
GFR - Is a blood test that checks how well the kidneys are functioning
Is measured by the amount of urea and creatinine in the blood
Why is creatinine level a better indicator of disease in GFR?
Better reflection of:
- Age
- Muscle mass
- Other underlying medical conditions
In a GFR test, what does the level of urea indicate?
Protein intake
Tissue catabolism
Stages of chronic failure
Stage 1 - GFR less than 90 ml per min
Stage 2 - 60-89 ml per min
Stage 3 - 3(a) GFR 45 - 59 ml per min
(b) 30-44 ml per min
Stage 4 - GFR 15-24 ml per min
Stage 5 - GFR less than 15 ml per min
Recognise the UK incidence of PKD
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Explain the underlying causes of its signs and symptoms
1.Blood in urine - because haemorrage of cysts and blood vessels
2.Pain and discomfort in the abdominal regions - enlarged kidneys
3.Subarachnoid hemmorrage - high BP / berry aneurysm
4.Hypertension - increased Renin release
5.liver cysts
6.Uremia (include itching / loss of appetite / gastric bleeding
This is due to platelet disfunction - this leads to inhibition of clotting
7.Symptoms of anemia (pail skin, fatigue)
8.Frequent urination - because decrease responsiveness of nephrons (collecting ducts) to ADH
9.UTI (urinary tract infection): because increased urinary tension
What is uremia?
Excessive urea in blood
Because kidneys do not remove it
State the main complications of PKD
Liver cysts - develop from peribillary glands and bile ducts epithelium
Cadriovascular complications - (Increases renin release so RAAS system activated,) high BP, this increases total peripheral resistance (vessels outside of heart) (TPR), increase TPR = increase afterload = more strain on left ventricle - left ventricular hypertrophy
Cardiovascular complication: increased fluid retention, due to decrease GFR, increase stretch of myocardium, therefore, left ventricular hypertrophy
Brain aneurysm - because of mutation of polycistin
Ankle edema - this is due to increase in protein loss in urine which reduces oncotic pressure, which leads to increased hydrostatic pressure and fluid leaving capillaries
State the underlying causes of the blood test abnormalities in PDK?
Explain the medical management of PDK with examples
Blood pressure control - ACe inhibitors, controlling the RAAS system
Also, angiotensin II receptor blockers
Pain management - OTC drugs (over the counter)
Antibiotic traitment
Diet modification
Surgey
Dialysis
Differentiate between nephrotic and nephritic syndromes
Nephrotic:
Increased protein in urea
Decreased albumin in blood
Nephritic
Blood in urine
Moderate amount of protein in urea
Hypertension
Describe the genetic basis of PKD
Two types with their distinct genetic basis:
Autosomal dominant polycystic kidney disease: Caused by mutations in the PKD1 or PKD2 genes coding for polycystin-1 and polycystin-2 respectively involved in the development and and function of kidney cells. Inherited in autosomal dominant pattern. Only One copy of the gene needs to be inherited to get the disease. 50% chance of passing the mutated gene to the next generation.
Autosomal recessive polycystic kidney disease: Caused by mutation in PKHD1 gene coding a protein called fibrocystin/ polyductin involved in development and function of kidney cells. inherited in an autosomal recessive pattern. One copy needs to be inherited by each parent to develop the disease. Parents do not have the disease themselves.
