Hypertension Flashcards
Hypertension doubles the risk of
CHD, CHF, stroke
Primary determinant of extracellullar fluid
Sodium
Modulate blood pressure over the short term
Adrenergic reflexes (Norepinephrine, epinephrine, dopamine)
Adrenergic reflexes are mediated by
G proteins and
Intracellular conc of second messengers
Alpha receptors are activated more by
Norepnephrine
Beta receptors are activated more by
Epinephrine
Located on postsynaptic cells in smooth muscle
Alpha 1 receptors
Causes vasoconstriction
➢ Increases renal tubular reabsorption of sodium
•α1 Receptors
Located on presynaptic membranes of postganglionic nerve terminals
α2 Receptors
Stimulates the rate and strength of cardiac contraction
Beta 1
By activation of epinephrine, it relax vascular smooth muscle
➢ Causes vasodilation
Beta 2
Mediated by stretch-sensitive sensory nerve endings in the carotid sinuses and the aortic arch
Arterial baroreflex
3 primary stimuli for renin secretion
- Decreased NaCl transport in the distal portion of the thick ascending limb of the loop of Henle
- Decreased pressure or stretch within the renal afferent arteriole (baroreceptor mechanism)
- Sympathetic nervous system stimulation of renin-secreting cells via β1 adrenoreceptors
Primary factor in regulating the synthesis and secretion of aldosterone
Angiotensin II
Mineralocorticoid
➢ Increases sodium reabsorption by amiloride-sensitive epithelial sodium channels (ENaC) on the apical surface of the principal cells of the renal cortical collecting duct
Aldosterone
Diagnosis of htn
Average of two or more seated blood pressure readings during each of two or more outpatient visits
the cardiovascular disease risk is doubled
For every 20mmHg increase in systolic and 10mmHg increase in diastolic,
Consequences of Hypertension
Cardiovascular disease
•Stroke
•Renal disease
•Peripheral or vascular disease
JNC 8 GUIDELINE
Normal <120 < 80
Pre 120-139/ 80-89
Stage 1 140-159/90-99
Stage 2 >/= 160/>/= 100
Isolated systolic htn
> /= 140/ <90
AHA HTN CATEGORIES
NORMAL <120/<80 ELEVATED 120-129/<80 HTN STAGE 1 130-139/80-89 HTN STAGE 2 140 OR HIGHER/ 90 OR HIGHER HTN CRISIS >180/ >120
AKA essential hypertension
Primary hypertension
80-95% of htn
Primary htn
Consequence of interaction between environmental and genetic factors
Primary hypertension
A specific, remediable cause of hypertension can be identified
Secondary hypertension
Clues for suspecting secondary HTN:
- Abrupt onset of htn
- Age of onset <20 or >50 y/o
- No family hx of htn
- Sudden inc in BP with stable stage 1 htn
- Poor bp control
- Systemic findings
- Disproporionate target organ damage
Secondary causes of htn
Renaal Primary aldosteronismm Cushing's syndrome 17 alpha hydroxylase deficiency Pheochromocytoma Aortic coarctation Obstructive sleep apnea Peeclampsia/eclampsia Hypothyroidism Hyperthyroidism Hypercalcemia Acromegaly
atleast three separate clinic-based measurements >140/90 mmHg
•At least two non-clinic-based measurements <140/90 mmHg in the absence of any evidence of target organ damage.
White coat htn
Normal BP in the office or clinic, but experiences episodes of INCREASED BP OUT OF THE OFFICE
Masked Hypertension
Office BP ≥ 140/90 and with ≥ 3 drugs at optimal doses
•Office BP <140/00 but requires ≥ 4 drugs
Resistant Hypertension
Dipping pattern
Nocturnal decrease in BP by 15% to 25% compared with awake values
Non dipping pattern
BP dec during sleep by 10% compared with awake
Increased BP during sleep, in a supine position
•A.K.A Rise Pattern
Reverse Dipping Pattern
A syndrome associated with an abrupt increase of blood pressure in a patient with underlying hypertension
Malignant Hypertension
Markedly elevated BP with target organ damage
Hypertensive emergency
