Hypertension Flashcards
RAAS system
Responds when BP serum sodium levels, or blood fluid levels are low by increasing BP
Angiotensinogen
Hormone in the blood that is released by the liver when BP is low
Renin
Enzyme released by the kidneys in response to angiotensinogen in the blood (decreased blood flow in the kidneys)
Angiotensin I
Created by reaction of angiotensinogen and renin, goes to the lungs and causes lungs to release ACE
ACE (angiotensin converting exyme)
Released by the lungs
Angiotensin II
ACE converts angiotensin I into angiotensin II and angiotensin II goes to the adrenal glands; also causes arterial vasoconstriction at the kidney level which increases BP
Aldosterone
Made when angiotensin II goes to the adrenal glands; increases sodium reabsorption which increases fluid and BP; decreases potassium thru urine excretion of K
Arginine vasopressin (ADH)
causes vasoconstrictor and water retention
Stress and BP
stress elevates angiotensin II–sets off RAAS
Arterial baroreceptors
in carotid sinus, aorta, L ventricle; sense BP and alter it by increasing HR; impacts vasodilation/constriction
Vasoautoregulation
helps keep consistent BP levels by altering resistance in BVs (based on MAP—mean arterial pressure)
Normal BP
Systolic under 120 AND diastolic under 80
Elevated BP
Systolic 120-129 AND diastolic under 80
HTN Stage 1
Systolic 130-139 OR diastolic 80-89
HTN Stage 2
Systolic 140+ OR diastolic 90+
HTN Stage 3
Systolic 180+ AND/OR diastolic 120+
What is BP known as
The silent killer
Primary HTN “essential HTN”
occurs w/o known cause; absence of underlying disease process; occurs because of interaction between genetics and environment, several neurohormonal effects
Factors involved in primary HTN
Overactive SNS due to obesity, insulin resistance; RAAS, inflammatory interleukins circulating, endothelial dysfunction, natriuretic peptides
Insulin resistance effect on BP
causes structural changes like permanent increase in peripheral vascular resistance
Natriuretic peptides
Cause renal sodium excretion (water retention); increased BP and fluid volume in peptides that are malfunctioning
Secondary HTN and causes
HTN with a known cause of underlying disease/dx like renal disease, adrenomedullary tumors (pheochromocytoma) which stimulate epinephrine, adrenocortical tumors which constantly secrete aldosterone and release angiotensin, and drugs (oral contraceptives, corticosteroids, antihistamines, cocaine, amphetamines)
S/S of HTN
None
When do you need to check BP immediately
End of organ damage
Long term outcomes of BP
Increased L vent work, inc risk of heart attack, L vent hypertrophy bc of excess cardiac demand, accelerated atherosclerosis, inc risk of aortic aneurysm, end-stage renal disease (inc SNS, RAAS, dec blood flow), higher risk of stroke aneurysm, and hemorrhage, retinopathy, retinal sclerosis, inc retinal eye pressure, inc tissue death, gangrene, intermittent claudication
Hypertensive crisis
complication of acute, uncontrolled BP; rapidly progressive HTN with systolic over 180 and/or diastolic over 120; often primary HTN; 2 types
Hypertensive urgency
no s/s of end organ damage caused by anxiety, pain, abrupt withdrawal of meds; treated with oral agents to gradually decrease BP with time
Hypertensive emergency
Leads to end organ damage; pt is symptomatic (headache, blurry vision); due to stroke, brain hemorrhage, chest pain, acute coronary; tx with IV meds in minutes to hours (even tho may cause future probs)
Angiotensin II is a….
Powerful vasoconstrictor
