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-defined as
-what is isolated HTN?
-what two factors influence development of HTN?
-what are some commonly associated conditions?

HTN defined as SBP greater than 140 or DBP greater than 90.

Isolated HTN is defined as SBP greater than 140 and DBP less than 90.

-often begins with thiazide diuretic
-elderly dont tolerate beta blockers, calcium channel blockers, or alpha blockers very well.
-ACEi only have to worry about renal artery stenosis..
-lifestyle changes

-volume of blood pumped into arterial tree
-stiffness of arteries


-each 20/10mmhg rise in BP above 115/75 _____ risk of CVD.

each 20/10mmhg rise in BP above 115/75 DOUBLES risk of CVD.


BP Classification: what is the SBP and DBP for each of the following:
-Stage 1 HTN
-Stage 2 HTN

Normal: less than 120/80

Prehypertension: 120-139/80-89

Stage 1 HTN: 140-159/90-99

Stage 2 HTN: greater than 160/100


Causes of secondary HTN

-when might we have 2nry HTN higher up on the DDX?

-sleep apnea
-drug induced (NSAIDS, steroids, birth control)
-Chronic kidney dz
-primary aldosteronism
-renovascular dz
-chronic steroid therapy or cushing syndrome
-Coarctation of the aorta
-thyroid or parathyroid dz

You might be more likely to think its secondary cause if the patient is younger and/or if its not being controlled with medications.


CVD Risk factors


Cigarette smoking


Obesity (BMI greater than 30)

Physical inactivity


MIcroalbuminuria or estimated GFR less than 60ml/min (normal is 90-120ml/min

Age (55+ for men, 65+ for women)

Family history of premature CVD


What organs are most likely to be damaged by HTN ?

-LVH *Independent risk factor for CVD*
-Angina or MI
-Coronary revascularization


Renal Dz

Peripheral artery dz



Lab test for HTN work up

EKG, UA, chem, fasting lipids, Hemoglobin, Hct, TSH, maybe microalbumin


Weight reduction of 10kg will decrease SBP by how much?

10kg weight loss will decrease SBP by 5-20mmhg


What are the initial drug choices for tx of each of the following:
-Stage 1 HTN
-Stage 2 HTN
-w/ compelling indications

What are the compelling indications?

Stage 1: Thiazide diuretics for most, consider ACEi, ARB, Beta blocker, Calcium Channel blockers, or combination

Stage 2: 2-drug combo for most (usually thiazide and ACEi, ARB, beta blocker, or calcium channel blocker. )

Compelling indications:
-diuretics, ACEi, ARB, Beta blocker, Calcium channel blockers as needed)

Prehypertension: no drugs indicated.

Compelling indications:
-Heart failure, S/P MI, High CAD risk, DM, chronic renal dz, recurrent stroke prevention


Home measurement of __/__ is generally considered HTN?

135/85 is usually considered HTN if taken at home.


What medications are used in initial therapy when treating HTN with each of the following compelling indications:
-heart failure
-High CAD Risk
-Chronic Renal Dz
-Recurrent Stroke prevention

Heart failure: Thiaz, Beta blocker, ACEI, ARB, ALDO ANT

S/P MI: Beta blockker, ACEI, ALDO ANT

High CAD risk: Thiaz, Beta blocker, ACEI, Calcium channel blocker

DM: Thiaz, beta blocker, ACEI, ARB, Calcium channel blocker

Renal Dz: ACEi, ARB

Stroke: thiaz, ACEI


Which HTN meds are good for each of the following:
-osteopenia, osteoporosis
-tachycardia, migraine, thyrotoxicosis, essential tremor, perioperative period

Osteopenia: thaizides

Tachycardia: beta blocker

Raynauds: calcium channel blocker

BPH: alpha-blockers


What is considered postural HTN?

What are the hypertensive emergencies?

What is pseudohypertension?

At what BP reading do you begin to see benefts of tx if your patient has isolated systolic hypertension? (ISH)

Postural HTN is defined as a drop in standing SBP greater than 10mmhg upon standing. Associated with dizziness/fainting

HTN emergencies: marked BP and acute Target organ damage.
-encephalopathy, TIA/CVA, papilledema, MI, pulmonary edema, aortic dissection, renal failure.

Pseudohypertension: falsely elevated BP readings d/t very stiff calcified arteries, commonly seen in the elderly.

Begin seeing benefits with treatment of ISH at SBP equal to or greater than 160mmhg. Benefits with tx of ISH when SBP is 140-160 are presumed but not proven.


What is a TIA?

What is a completed stroke?

What is the MC artery affected by strokes?

TIA: brief episodes of focal neurological deficits lasting 2-3minutes to at most a few hours but no longer than 24hrs leaving no residual deficits with complete functional recovery.

acute, sustained functional neurological deficit lasting from days to permanent.

MC artery affected is the middle cerebral artery.


Anterior or Middle cerebral artery Stroke:
-affected area of body

What is amaurosis fugax?

affected areas: face-hand-arm-leg contralateral hemiparesis

Amaurosis fugax: -monocular blindness cause from transient ischemia to the occular artery. if those doesnt go away it becomes CRAO.


Middle Cerebral Artery Occlusion:
-affected area of body

contralateral hemiplegia in face-arm-hand

Sx: aphasia(left), Right = confusion, spatial disorientation, sensory and emotion neglect.


Anterior Cerebral artery occlusion:
-affected area of body?

sensorimotor deficit in contralateral foot and leg

Sx: brocas or anterior conduction aphasia in dominant hemisphere

TIAs rarely affect ACA distribution


Posterior Stroke TIA/Stoke
-sensorimotor deficits

-diplopia/dysconjugate gaze, ocular palsy, homonymous hemianopsia

Sensorimotor deficits: ipsilateral face and contralateral limbs, drop attack (rarely TIA)


Hemorrhagic Stroke

-seriously ill
-deteriorate more rapidly and have HA, n/v, and decreased consciousness as prominent signs


Subarachnoid Hemorrhage
-physical signs

-rupture of an artery with bleeding onto the surface of the brain


-"worst HA ever" that radiates to face and neck
-progresses to maximal intensity immediately after onset

Physical Signs
-nuchal rigidity
-altered mental status
-poor sign if associated with transient loss of consciousness, may represent a complicating factor such as sz or cardiac dysrhymia


Intracerebral Hemorrhage

-rupture of an artery with bleeding into the brain parenchyma


-any of the signs/sx of ischemic stroke



-ABCs, H&P
-EKG, pulse ox
-cbc, electrolyte, glucose, ABG, PT/PTT, urine drug screen, LP
-CT/MRI head scan
-Echo, EEG
-Carotid duplex US
-MRA or angiography

--prevention/lifestyle modification
--early recognition
--ABCs, O2, IV
--TPA (must be administered within 3hrs of onset of signs and sx)
-surgical- carotid endarterectomy


Thrombolytic CI

CI in:
-BP greater than 185/110
-Acute MI
-LP within 7 days
-arterial puncture at incompressible site
-surgery within 14days
-bleeding diathesis
-within 3mo of head trauma
-hx of intracranial hemorrhage
-minor or rapidly improving stroke sx


Stroke Management

Acute or chronic anti-platelet therapy:
-ASA 81mg vs 325mg

Chronic prophylactic anticoagulation:

Psychiatric services


VNS/Home health attendant

skilled nursing facility

social services


Parkinsons Disease:
-what is this?
-triad of sx

What: an idiopathic slowly progressive degenerative CNS disorder.

-tremor, muscular rigidity, bradykinesia

Cause: deficient dopamine from the substansia nigra

-hx and PE
-dx clinically if 2 of the 3 cardinal features (tremor, rigidity, bradykinesia)

-sx begin typically in one extremity or one side
-stiffness/slowed movements
-tremor or shakin at rest
-diff getting out of chair
-frequent falls
-diff walking
-memory los s
-speech changes (whispering. rapid speech)
-smalll handwriting
-slowness in performing activity
-sialorrhea (drooling)


-PE findings

-muscle rigidity, cog wheeling
-postural instability
-decreased arm swinging in ambulation
-masked facies
-resting tremor/pill rolling
-dysarthria, hypokinetic, monotonus volume
-painful dystonia
-akathisia (inability to sit still)
-seborrheic dermatitis face and scalp
-orthostatic hypotension

-Sinemet (Carbidopa/levodopa) OR dopamine agonists
-MOAB inihibtors
-deep brain stimulation
-constipation prophylaxis with dietary fiber, fruit juices, sometimes laxatives
-regular exercise program


Polymyalgia Rhematica
-MC characterized characterized by?
-MC in what age?
-other sx

Characterized by severe bilateral pain and morning stiffness of the shoulder, neck, and pelvic girdle.

MC in people over 50YO, peaks 70-80YO.

Cause: unknown, but may be linked to HLA-DRBI *04 and *01 alleles
-a viral or infectious cause has also been suspected d/t increased prevalence of abys to respiratory syncitial virus (RSV) and adenovirus .

-the ones mentioned above and...
--pain on active and passive movment of joints
--morning stiffness of more than 1hr and also after periods of rest
--loss of weight
--joint effusions
-- +/- assymmetric peripheral arthritis, carpal tunnel, edema of hands, wrists, ankles, and feet.


Polymyalgia Rheumatica:
-associated diseases

-ESR**** (40-100mm/hr)
-IL-6 usually raised
-CBC: normochromic, normocytic anemia
-Rheumatoid and ANA not elevated
-LFTs mildly elevated

Associated disease:
-Giant cell arteritis can co-exist in about 30% of patients with PMR.

-prednisone is DOC!
--15mg/day; produces dramatic response, a pt who was severely crippled may regain mobility and full independence after one week.
-alternatives include: bisphosphonates

*calcium and Vit D supplementation should be given to all PMR patients who are receiving prednisone.

-physiotherapist and OT


Polymyalgia Rheumatica:

-responds well to tx w/ steroids resulting in remission.
-relapse may occur usually within 2 years of stopping steroids, but the condition remains steroid responsive.