Patho Exam 5

LAST ONE Urogenitary and Endocrine Justin McGraw D'Youville University

osmolarity

plasma sodium concentraton

osmoregulation controlled by

water intake and excretion

volume regulation controlled by

sodium retention and excretion

osmoregulation and volume regulation

controlled independently

dehydration

most common disturbance of H2O balance from inadequate intake or excessive H2O loss

Overhydration

less common disturbance of H2O balance, from excessive fluid intake when renal function is impaired

hypovolemia

decrease in plasma volume and loss of blood pressure

principle extracellular ions (electrolytes)

sodium, chloride, and bicarbonate

principal intracellular ions

potassium, magnesium, and phosphate

neutral

overall electrical charge in both intracellular and extracellular fluid compartments

regulation of plasma pH depends on

regulation of bicarbonate and dissolved carbon dioxide

kidneys reabsorb and manufacture

bicarbonate

amount of dissolved carbon dioxide controlled by

respiratory rate

kidney excretes

acid metabolic products

Acidosis

blood pH acidic from excessive carbonic acid or reduced bicarbonate

Alkalosis

blood pH basic from decreased carbonic acid or increased bicarbonate

metabolic

disturbance in acid-base balance due to bicarbonate

respiratory

disturbance in acid-base balance due to carbonic acid

metabolic acidosis

increased endogenous acid buffered by bicarbonate causes levels to fall

compensation for metabolic acidosis

hyperventilation to lower PCO2 and increase bicarbonate production in kidneys

respiratory acidosis

increased H2CO3 concentration from inefficient CO2 excretion by lungs

metabolic alkalosis

increased plasma bicarbonate with potassium deficiency from loss of acids

metabolic alkalosis compensation

inefficient, requires simultaneous correction of potassium deficiency

respiratory alkalosis

reduced H2CO3 concentration from hyperventilation, excess bicarbonatere

respiratory alkalosis compensation

excretion of bicarbonate by kidneys

CO2 concentration

increased respiration lowers this to make blood more alkaline

decreased respiration elevates this to raise plasma carbon dioxide

alveolar PCO2

renal pyramid

inner medulla of kidneys

renal columns

outer cortex of kidneys

kidneys excrete waste products of food metabolism

CO2 and H2O, Urea and other acids

kidneys regulate mineral and H2O balance

excrete excess, conserve as required

body’s internal environment determined by what

the kidneys retain

erythropoietin and renin

regulate RBC production and blood pressure

erythropoietin

regulates red blood cell production in bone marrow

ureter

conveys urine into bladder by peristalsis

renal pelvis

expanded upper portion of ureter

major calyces

subdivisions of renal pelvis

minor calyces

subdivisions of major calyces into which renal papillae discharge

bladder

stores urine, discharges into urethra during voiding

urethra

conveys urine from the bladder for excretion

nephrons

basic unit of kidney made up of glomerulus and renal tubule

how many nephrons in each kidney

about 1 million

glomerulus

tufts of capillaries in kidney filters blood to form urine

inner glomerulus

fenestrated capillary endothelium

middle glomerulus

basement membrane

outer glomerulus

capillary endothelial cells (with foot processes and filtration slits)

mesangial cells

contractile phagocytic cells holding capillary tuft together

mesangial cells regulate caliber of capillaries affecting

filtration rate

control rate of glomerular filtration

GFR

increased arterial pressure

increases resistance (tone) of afferent arteriole of glomerulus regulating GFR

macula densa (in loop of Henle)

senses increased pressure in afferent arteriole and increases tone to regulate GFR

high plasma osmolarity sensed in

hypothalamus

high plasma osmolarity symptoms

thirst and secretion of anti diuretic hormone (ADH) from posterior pituitary

hypoperfusion of kidney

low blood pressure or volume

hypoperfusion of kidney sensed by

juxtaglomerular cells in the walls of the afferent glomerular arteriole

hypoperfusion results in

renin release into the blood and activiation of RAAS

RAAS

renin-angiotensin-aldosterone system

what does RAAS and renin do

regulate systemic blood pressure

renin

released in response to decreased blood volume, low blood pressure, low sodium

angiotensin I converted into angiotensin II by

angiotensin converting enzyme (ACE) as blood flows through the lungs

Angiotensin II

powerful vasoconstrictor increasing fluid in vascular system and raising blood pressure

angiotensin II raises blood pressure by causing

peripheral arterioles to constrict

angiotensin II stimulates aldosterone secretion from adrenal cortex

increases reabsorption of NaCl and H2O by kidneys

renal regulation of blood pressure system

self regulating

renal tubule

reabsorbs most of filtrate., secretes unwanted components into tubular fluid, regulates H2O balance

proximal end of renal tubule

bowman capsule

distal end of renal tubule

empties into collecting tubules

kidneys arise from

mesoderm

kidneys develop here before ascending to final position

pelvis

bladder derived from

lower end of intestinal tract

excretory ducts (ureters, calyces, pelves) develop from

ureteric buds that extend from bladder into the developing kidneys

renal angenesis

failure of one or both kidneys to develop

bilateral renal angensis

rare, associated with other congenital anomalies, incompatible with life

unilateral renal agenesis

common, asymptomatic, other kidney enlarges to compensate

duplications of urinary tract

complete and incomplete duplication

complete duplication

formation of extra ureter and renal pelvis

incomplete duplication

only upper part of excretory system is duplicated

malposition renal abnormality

one or both kidneys, associated with fusion of kidneys; horseshoe kidney; fusion of upper pole

renal failure

inability of kidneys to regulate and excrete

uremia associated with

retention of urea in blood, metabolic acidosis, ketosis

end stage of many kidney diseases

uremia

chronic renal disease

renal function fails as number of functioning nephrons declines to 30% of normal, remainders work harder at higher blood pressure and are injured

how long does renal function have to be abnormal before it is chronic renal disease

over three months

End Stage Renal Disease (ESRD)

results in uremia, complete kidney failure, requires dialysis or transplant to live

hypertensive nephrosclerosis

renal arterioles undergo thickening from carrying blood at a much higher pressure than normal

hypertensive nephrosclerosis results from

severe hypertension

hypertensive nephrosclerosis causes

chronic renal disease

hypertensive nephrosclerosis progressive

reduced glomerular filtration, kidneys shrink, possibly ESRD

Diabetic Nephropathy

thickening of glomerular basement membranes, complication of long-standing diabetes

how many ESRD patients have type II diabetes

half

manifestations of diabetic nephropathy

progressive impairment of renal function, nephrotic syndrome from protein loss, may cause ESRD

diabetic nephropathy treatment

no specific treatment can arrest progression of disease

End Stage Renal Disease (uremia)

retention of excessive by-products of protein metabolism in the blood

ESRD fluid, electrolyte, acid-base regulation fail

metabolic acidosis occurs, lack of erythropoietin leads to anemia

level of urea in blood (blood urea nitrogen BUN)

measurement of severity of renal failure

clinical manifestations of ESRD

weakness, loss of appetite, nausea, vomiting, anemia, HTN

ESRD treatment

hemodialysis, transplantation

hemodialysis

substitutes for function of kidneys by removing waste products from patients blood across a semipermeable membrane into a solution

solution used for hemodialysis

dialysate

extracorporeal dialysis

more common, patients circulation connected to artificial kidney machine