Hypertension And diabetes Insipidus Flashcards Preview

Renal Course > Hypertension And diabetes Insipidus > Flashcards

Flashcards in Hypertension And diabetes Insipidus Deck (14)
Loading flashcards...

How do kidneys influence peripheral resistance?

Through RAAS

Renin is released by renal juxtaglomerular cells in response to:
- low blood pressure in afferent arterioles
- elevated Catecholamines in blood
- low sodium levels in DCT (low GFR)


RAAS pathway review

1) renin gets secreted via that PCT cells in the kidneys in response to low BP/hypo-perfusion of the kidneys

2) renin cleaves angiotensinogen from the liver into angiotensin-1

3) angiotensin-1 gets cleaved by the lungs into angiotensin-2

4) angiotensin-2 vasoconstriction blood vessels and promotes aldosterone release in the adrenal glands

5) aldosterone goes to the DCT and increases sodium reuptake/ water up take and increases blood volume while also secreting K+ and H+ ions


Essential HTN

Results from interplay of genetics and environmental factors which casues increased blood volume and/or peripheral resistance
- often is asymptomatic for years

*Is always formed by the contribution of altered renal sodium handling (increased sodium resorption in the presence of normal arterial pressure) and increased vascular resistance*


HTN definition and epidemiology

- nearly 50% of all people are hypertensive

Increases with age and also in African Americans

Roughly 50% of untreated HTN cases die from ischmic heart disease/CHF or stroke

95% of cases are idiopathic or essential
- other 5% is renal artery stenosis of hyperaldosteronism
- essential HTN is caused by a combination of altered renal sodium handling and increased vascular resistance


Renal artery stenosis

Causes HTN due to chronic decreased GFR and pressure Blood flow to the kidney via afferent arteriole
- produces chronic renin release since the kidney assumes the body is hypotensive


Single gene disorders that can produce rare forms of HTN

1) aldosterone metabolism genes
- aldosterone synthase/11B-hydroxylase/ 17a-hydroxylase
- leads to hyperaldosteronism

2) genes related to proteins that influence sodium reabsorption
- Liddle syndrome (gain of function in Na+ channels in the DCTs)


The 3 forms of small vessel changes that leads to HTN

1) hyaline arteriolosclerosis
- causes benign HTN
- marked by thick pink hyaline thickening of the arteriolar wall as and luminal narrowing
- stem from plasma components leaking across injured EC into vessel walls and increased ECM production
- common in older patients, patients with chronic NON-SEVERE HTN or diabetic patients

2) hyperplastic arteriolosclerosis
- causes SEVERE HTN
- vessels show “onion-skin” and concentric laminated thickening of the arteriolar walls

3) necrotizing arteriolitis
- casues malignant HTN/ caused by malignant HTN


Oral and neural component of the pituitary gland

Oral = outpocketing of the ectoderm from the roof of the primitive mouth
- forms the hypophyseal pouch of the pituitary gland and the anterior adenohypophysis

Neural = neurohypophyseal bud growing down from the floor of the future diencephalon as the infundibulum that attaches to the brain
- for a the posterior neurohypophysis

**because of this, the pituitary gland can actually be considered two separate glands in 1
- posterior neurohypophysis
- anterior adenohypophysis**


What hormones are secreted via the pituitary that function in blood pressure and blood volume

ADH hormone (arginine vasopressin)
- is released in response to increased blood tonicity via the osmoreceptors in the hypothalamus
- secreted via supraoptic neurons
- function = increases permeability of the collecting ducts to water and allows reabsorption of water

- stimulates contractions of mammillary glands and uterine smooth muscle cells


Diabetes insipidus

Caused by underlying ADH deficiency
- polyuria is seen since the kidney cant reabsorb water properly

- polyuria
- polydipsia
- excessive thirst

Caused by
- head trauma
- tumors
- inflammatory disorders
- surgical complications
- idiopathic

**can be central or nephrogenic**
- central = not releasing enough ADH
- nephrogenic = DCT/CD cells dont respond to ADH (but there are normal levels)

Both types present with increased serum sodium and osmolality and very dilute urine with low specific gravity


Syndrome of inappropriate ADH

Too much ADH being produced causes excess water reabsoption and produces decreased serum osmolaitiy and sodium concentration (hyponatremia)
- also cerebral edema and neurological symptoms
- **TBW is increased but blood volume remains NORMAL (peripheral edema does not develop since water goes into the intracellular space)**

- head trauma
- cancer
- certain medications


Blood pressure is a function of what?

Cardiac output and peripheral vascular resistance

Cardiac output = stroke volume x heart rate

Peripheral resistance = arteriole resistance and vasomotor tone


how does atrial naturetic peptides work?

Get released in response to high levels of blood (volume expansion)
-essentially reverses aldosterone effects (inhibits sodium reabsorption and retains K+)
- also induces vasodilation


Malignant HTN

Accounts for 5% of HTN patients

Shows rapidly rising BP that if left untreated leads to death within 1-2yrs

Usually presents with severe HTN (> 180/120) and frequently shows renal failure signs and retinal hemorrhages

Also often superimposed on preexisting benign HTN