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Geriatrics > HTN, CVD, Parkinsons, Polymyalgia > Flashcards

HTN, CVD, Parkinsons, Polymyalgia Flashcards

1
Q

What is HTN? ISH?

A
  • Systolic over 140 or diastolic over 90
  • isolated systolic HTN (ISH) is common form of HTN in elderly, systolic over 140 and diastolic below 90
  • for most elderly pts, HTN doesn’t have a reversible cause and is asx
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2
Q

What should eval of HTN include? Tx?

A
  • eval should include detection of other cardiovascular risk factors and end organ damage and a seach for secondary causes when appropriate
  • tx w/ lifestyle modifications and drugs, often starting w/ thiazide diuretic
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3
Q

How common is HTN in people older than 80?

A
  • 65%
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4
Q

What are the major mechanisms of BP regulation?

A
  • volume of blood pumped into arterial tree - this is determined by
    A: vol of blood w/in the heart
    B: vigor of heart’s contraction
    C: kidneys
  • stiffness of the arteries - this is determined by:
    A: vascular smooth muscle cell contractile tone
    B: endothelial cell fxn
    C: matrix that embeds the vascular smooth muscle cells
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5
Q

What are assoc conditions of HTN?

A
  • MI
  • CVA
  • PVD
  • CHF
  • Renal Failure
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6
Q

Risk of CVD and relationship w/ BP?

A
  • independent of other risks

- if 115/75 is ideal - each 20/10 mmHg rise doubles risk of CVD

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7
Q

What is preHTN?

A
  • SBP: 120-139
    or
  • DBP: 80-89
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8
Q

What are the benefits of lowering BP?

A
  • stroke incidence: reduction of 35-40%
  • MI: 20-25%
  • Heart failure: 50% (long standing HTN is MC cause of diastolic heart failure)
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9
Q

Dementia relationship w/ HTN?

A
  • cognitive impairment more common w/ HTN

- reduced progression of dementia occurs w/ effective antiHTN therapy

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10
Q

Causes of secondary HTN?

A
  • sleep apnea
  • drug induced
  • chronic kidney disease
  • primary aldosteronism
  • renovascular disease
  • chronic steroid therapy or cushing’s syndrome
  • pheochromocytoma
  • coarctation of the aorta
  • thyroid or parathyroid disease
  • think about a secondary cause if uncontrollable still w. meds or in younger pt
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11
Q

What are CVD risk factors?

A
  • HTN
  • cigarette smoking
  • dyslipidemia
  • obesity (BMI greater than 30 kg/m2)
  • physical inactivity
  • DM
  • microalbuminuria or est GFR of less than 60ml/min
  • age: 55+ for men and 65+ for women
  • family hx of premature CVD )(men younger than 55 and women less than 65)
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12
Q

Target organ damage - from HTN/CVD?

A 
- heart:
LVH
angina or prior MI 
prior coronary revascularization
CHF
- CVA/TIA
- renal disease
- PAD
- retinopathy
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13
Q

Assoc of LVH and CVD? How can we stop this from progressing?

A
  • LVH is an independent RF for CVD
  • regression of LVH occurs w/ aggressive BP management: wt loss, Na restriction, and tx w/ all classes of drugs except the direct vasodilators hydrazine and minoxidil
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14
Q

Lab tests for HTN?

A 
always:
EKG
UA
Chem
fasting lipid panel
H/H, TSH

optional:
microalbumin

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15
Q

Diff lifestyle modifications for HTN?

A
  • wt reduction 5-20 mmHg/10kg wt loss
  • DASH eating plan 8-14 mmHg
  • Na restriction 2-8mmHg
  • physical activity: 4-9 mmHg
  • moderation of ETOH consumption: 2-4 mmHg
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16
Q

Initial drug choices in HTN?

A

w/o compelling indications:

  • stage 1: SBP 140-159 or DBP 90-99 mmHg - thiazide type diuretics, may consider ACEI, ARB, BB, CCB or combo
  • stage 2: SBP over 160 or DBP over 100 - 2 drug combo for most: usually thiazide and ACEI or ARB, BB or CCB

w/ compelling indications:
other antiHTN drugs - diuretics, ACEI, ARB, BB, CCB as needed

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17
Q

84 yo shows up to Urogyn clinic for appt and has BP of 190/100 and is asx- what should you do?

A
  • send her to ER

- ask if she has HA, blurry vision, sxs of MI

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18
Q

What could a lack of BP drop of 10-20% during the night indicate?

A
  • possible increased risk for CV events
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19
Q

What home BP measurement is considered HTN?

A
  • over 135/85
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20
Q

What should you do if BP is over 20/10 mmHg above goal?

A
  • start w/ 2 agents
  • one should be thiazide
  • most will reqr more than 1 drug to achieve goal BP
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21
Q

Initial therapy for HTN w/ heart failure?

A

THIAZ, BB, ACEI, ARB, ALDO ANT

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22
Q

Initial therapy for HTN w/ S/P MI?

A
  • BB, ACEI, ALDO ANT
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23
Q

Initial therapy for HTN w/ high risk of CAD?

A
  • THIAZ, BB, ACEI, CCB
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24
Q

Initial therapy for HTN w/ diabetes?

A
  • THIAZ, BB, ACEI, ARB, CCB
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25
Q

Initial therapy for chronic renal disease and HTN?

A
  • ACEI and ARB
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26
Q

Initial therapy for recurrent stroke prevention in pt w/ HTN?

A
  • THIAZ, ACEI
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27
Q

What other diseases are thiazides therapeutic for?

A
  • osteopenia/osteoporosis
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28
Q

Other uses for BBs?

A
  • atrial tachycardias, migraine, thyrotoxocosis, essential tremor, perioperative period, peformance anxiety
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29
Q

Other use for CCBs?

A
  • raynauds
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30
Q

Other use for Alpha-blockers?

A
  • useful in BPH
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31
Q

Relative CIs for antiHTN drugs?

A
  • thiazides: gout, hx of hyponatremia
  • BB: RAD or 2nd/3rd degree Heart block
  • ACEI/ARBs: risk of preg
  • Aldosterone antag/K sparing diuretics: hyperkalemia
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32
Q

What is postural hypotension? When should orthostatics be checked?

A
  • drop in standing SBP of over 10 mmHg, assoc w/ dizziness/fainting
  • always check these when adjusting meds
  • avoid vol depletion and excessively rapid titration
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33
Q

What are HTN emergencies?

A
  • marked BP elevations and acute TOD:
    encephalopathy, TIA/CVA, papilledema, MI or unstable angina, Pulmonary edema, life threatening arterial bleeding or aortic dissection, renal failure
  • this reqr hospitalization and parenteral drug therapy
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34
Q

What are HTN urgencies?

A
  • marked BP elevation but no acute TOD
  • usually doesn’t reqr hospitalization
  • does reqr immediate combo oral antiHTN therapy
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35
Q

MC HTN in geri population? Cause of this?

A
  • ISH: more than 2/3 of cases
  • caused primarily by an increase in arterial stiffness due to increased collagen deposition and cross linking, degeneration of elastin fibers, atherosclerotic changes, and age related endothelial dysfxn
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36
Q

When would BP reading be falsely elevated in elderly pts?

A
  • if they have really stiff, calcified arteries - known as pseudoHTN
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37
Q

Tx of ISH when systolic is greater than 160 reduces incidence of what?

A
  • MI, stroke and HF
38
Q

in elderly - all cause mortality rates increase when DBPs are in what ranges?

A
  • DBP: over 80

- DBP: under 60

39
Q

Goal for BP in elderly? What should you eval for?

A
  • goal: under 140/90
  • eval for:
    target organ damage
    other CV RFs
40
Q

How common is cerebrovascular disease?

A
  • 3rd leading cause of death and disability in developed world exceeded only by heart disease and cancer
  • each yr: 750,000 Americans have a stroke, and about 150,000 die
  • declining incidence w/ better tx of HTN and reduction in smoking
  • at any time, there are 2 mill stroke survivors in the US
  • stroke incidence and mortality rate increases w/ age, especially after 65: 88% of persons who die of stroke are older than 65
  • higher among men and blacks
41
Q

What are complications of a stroke?

A
  • stroke activates clotting system, potentially leading to venous thromboembolism and MI during the acute period or during convalescence
  • sometimes hard to determine whether MI or brain ischemia came first
42
Q

Major RFs for a stroke?

A
  • HTN (systolic or diastolic)
  • smoking
  • A fib
  • MI
  • hyperlipidemia
  • diabetes
  • CHF
  • acute alcohol use
  • TIA w/ over 70% occlusion of carotid arteries
  • OCPs when combined w/ smoking in women
  • hypercoagulopathy (factor 5 leiden, post op pts)
  • higher RBC count and hemoglobinopathy (polycythemia)
  • age, gender, race, prior stroke, hereditary
43
Q

Classification of a stroke?

A
  • ischemic (75% of strokes - due to embolus or thrombosis)

- hemorrhagic

44
Q

What is a TIA?

A
  • brief episodes of focal neuro deficits lasting 2-3 min to at most a few hrs but no longer than 24 hrs leaving no residual deficits w/ complete fxnl recovery
  • over 75% of TIAs last less than 5 minutes
  • can be warning sign of impending stroke - about 1/3 of persons who have had a TIA will have a stroke
45
Q

What is a completed stroke?

A
  • acute, sustained, fxnl neuro deficit lasting from days to permanent. There is necrosis or infarction in at least a part of area supplied by the affected artery
46
Q

MC blocked artery in a stroke?

A

-Middle cerebral artery

47
Q

What does stroke presentation depend on?

A
  • on affected vessel and whether or not there are any further complicating factors
48
Q

Diff stroke syndromes (location of affected vessel)?

A
  • ICA occlusion
  • ACA occlusion
  • MCA occlusion
  • OCA occlusion
  • verterbrobasilar occlusion
  • lacunar infarct
  • spinal stroke
49
Q

Presentation of anterior circulation TIA/stroke?

A
  • anterior or middle cerebral artery involved
  • amaurosis fugax (monocular blindness)
  • face-hand-arm-leg contralateral hemiparesis
  • aphasia/dysarthria
50
Q

Presentation of MCA occlusion?

A
  • similar to ICA-mCA occlusion
  • contralateral hemiplegia in face-arm-hand
  • dominant hemisphere = aphasia
  • nondominant R hemisphere = confusion, spatial disorientation, sensory and emotional neglect
51
Q

Presentation of ACA occlusion?

A
  • sensorimotor deficit in contralateral foot and leg
  • brocas or anterior conduction aphasia in dominant hemisphere is possible (deep frontal lobe nuclei)
  • TIAs rarely affect ACA distribution
52
Q

Presentation of posterior TIA and stroke?

A
  • vertigo
  • diplopia/dysconjugate gaze, ocular palsy homonymous hemianopsia
  • sensorimotor deficits - ipsilateral face and contralateral limbs, drop attack (rarely TIA)
  • dysarthria
  • ataxia
53
Q

Presentation of vertebro-basilar posterior circulation occlusion?

A
  • emboli less frequent in posterior circulation but more common anterior
  • various syndromes depending on site of occlusion
  • VA-PICA syndrome - HA, ataxia, N/V, paralysis in tongue and swallowing all ipsilateral, ipsilateral face and contralateral body. Horner’s sydrome
  • PICA-AICA-SCA acute cerebellar infarction
  • V-B jxn: lower extremity paraplegia or tetraplegia, conjugate or dysconjugate gaze paralysis, constricted pupils, respiratory depression, coma
  • basilar apex: hemiplegia-diplegia, pupillary and oculomotor paralysis, visual field defectds, stupor and coma
54
Q

Spinal stroke presentation?

A
  • rare
  • anterior spinal artery
  • assoc w/ prolonged hypotension and intraspinal mass lesions
55
Q

What is a lacunar infarct? Presentation?

A
  • small, deep infarcts caused by occlusion of small arteries that penetrate deeper brain structures (internal capsule, thalamus, pons)
  • often sxs are subtle and aren’t noticeable until there are multiple cumulative events
56
Q

Diff hemorrhagic strokes? Presentation?

A
  • subarachnoid hemorrhage
  • intracerebral hemorrhage
  • in general - pts w/ hemorrhagic stroke present seriously ill. Deteriorate more rapidly and have HA, N/V, and decreased consciousness as prominent signs
57
Q

Types of intracerebral hemorrhages?

A
  • HTN atherosclerotic hemorrhage, lobar hemorrhages, hemorrhage from vascular malformations and uncommonly bleeding into brain tumors, blood dyscrasias or anticoag, and inflammatory vasculopathies
58
Q

Cause of subarachnoid hemorrhage? How common?

A
  • rupture of artery w/ bleeding onto surface of brain
  • accounts for 10% of all strokes but for much higher % of deaths due to stroke
  • # 1 cause is aneurysm, AVM (85% from congenital berry aneurysm, 10% cause not found
  • may also be a result of bleeding disorder due to anticoags - bad combo
  • 25% of pts may have warning leak sxs
59
Q

signs and Sxs of subarachnoid hemorrhage?

A
  • worst HA ever in pts life radiates to face and neck, progresses to max intensity immediately after onset
  • phonophobia or photophobia
    signs:
    nuchal rigidity
    alt mental status
    poor sign if assoc w/ transient loss of consciousness, may represent a complicating factor such as a seizure or cardiac dysrythmia
  • papilledema
  • may not have neuro defect
60
Q

DDx of a stroke?

A
  • focal seizures
  • glaucoma
  • benign vertigo or meneires disease
  • cardiac syncope or syncope from other causes
  • migraine HA
  • intracranial neoplasm
  • subdural hematoma
  • epidurla hematoma
  • hyperglycemia (NHH, DKA), hypoglycemia
  • post cardiac arrest ischemia
  • drug overdose
  • meningitis, encephalitis
  • trauma
  • anoxic encephalopathy
  • hypertensive encephalopathy
61
Q

Causes? Presentation of a intracerebral hemorrhage?

A
  • rupture of artery w/ bleeding into brain parenchyma - number 1 cause is HTN, amyloid angiopathy
  • these pts can present w/ any signs and sxs of ischemic stroke
  • HTN atherosclerotic hemorrhage usually involves basal ganglia, thalamus, cerebellum, and pons - often large and catastrophic - found in hypertensives 60% of time, degenerative atherosclerotic vascular inhury
  • lobar hemorrhages are smaller
62
Q

Dx of a stroke?

A
  • ABCs
  • H and P (including RF assessment and thorough description of sxs/deficits, meds, PMHx, PSHx, time of onset, duration, a thorough neuro exam
  • EKG, monitor, pulse oximetry
  • labs (CBC, electrolytes, glucose, ABG, PT/PTT, urine drug screen, LP)
  • CT or MR head scan
  • echocardiography, EEG
  • carotid duplex US
  • MRA or angiography
63
Q

Management of an acute stroke?

A

medical management:
- prevention, lifestyle modification, early recognition w/ rapid transport/pre arrival notification
- ABCs, O2, IV
- rapid eval for fibrinolytic therapy (tPA)
surgical management
prognosis

64
Q

Are anticoag indicated in acute setting of a stroke?

A
  • no, recent studies have shown no short or long term benefit of admin heparin for acute ischemic stroke
65
Q

Use of tPA for stroke?

A
  • intra arterial and intravenous

- only tPA approved for ischemic stroke if given w/in 3 hrs of onset of signs and sxs of Class I AHA recommendation

66
Q

CI to thrombolytics?

A
  • if BP over 185/110, AMI, seizure, hemorrhage, LP w/in days, arterial puncture at incompressible site, surgery w/in 14 days, bleeding diathesis, w/in 3 months of head trauma, hx of intracranial hemorrhage, minor or rapidly improving stroke sxs
67
Q

Acute or chronic prophylactic anti-platelet therapy?

A
  • role of ASA (81 mg vs 325 mg)

- Plavix (not Ticlodipine)

68
Q

When is chronic proph. anticoag indicated?

A
  • in acute wall MI w/ mural thrombus formation (continue heparin/warfarin until thrombus dissolves). INR
  • chronic a fib w/ any or all of the following RFs: CHF w/in 3 months, HTN, previous thromboembolism, LV dysfxn and or enlarged left atrium, chronic valvular disease. A fib w/o any of the following RFs may be tx w/ chronic ASA therapy
69
Q

Chronic management for pts who suffered a stroke?

A
  • multidisciplinary approach
  • psych services
  • PT/OT/ speech language
  • VNS/home health attendant
  • skilled nursing facility
  • social services
  • family support groups
70
Q

When is a carotid endartectomy indicated?

A
  • good general health
  • HTN controlled
  • internal carotid stenosis 70-99%
  • ipsilateral stroke or TIA w/in 3-6 months
  • surgeon w/ morbidity/mortality less than 2%
  • worse outcome if used to tx evolving stroke
71
Q

What is parkinson’s disease? Characterized by?

A
  • idiopathic, slowly progressive degenerative CNS disorder that is characterized by:
    tremory (resting)
    muscular rigidity
    bradykinesia
  • strial dopamine is deficient and dopaminergic neurons are lost in substantia nigra
  • affects about 0.3% of general pop:
    3% are older than 65, 10% are older than 80
  • common cause of disability in elderly
72
Q

What else may parkinson’s pts develop? What else may cause this?

A
  • dementia

- similar sxs (called parkinsonism) may occur secondary to other disorders, drugs (esp antipsychotics) or toxins

73
Q

Dx parkinson’s?

A
  • by H and P
  • dx clinically if 2/3 cardinal features (tremor, rigidity, bradkinesia) are present
  • sxs and signs typically begin in one extremity or one side but eventuall involve other limbs and trunk
74
Q

Sxs reported by parkinson’s pts?

A
  • stiffness and slowed movements
  • tremor or shaking at rest
  • difficulty getting out of chair or rolling in bed
  • frequent falls or tripping
  • difficulty walking
  • memory loss
  • speech changes (whispering, rapid speech)
  • small handwriting
  • slowness in performing activities od daily living
  • sialorrhea
75
Q

Physical findings in parkinson’s disease?

A
  • hands initially affected but legs, chin, and head are involved w/ advanced disease
  • muscle rigidity, cog wheeling type
  • bradykinesia
  • postural instability, assumes a stopped forward posture
  • decreased arm swinging in ambulatory activity
  • resting tremor/pill rolling
  • masked facies
  • micrographia
  • dysarthria, hypokinetic, monotonous low volume
  • painful dystonia
  • dementia
  • depression up to 50%
  • akathisia inability to sit still
  • seborrheic dermatitis - face and scalp
  • autonomic dysfxn: orthostatic hypotension
76
Q

DDx for parkinson’s?

A
  • progressive suprnuclear palsy
  • multisystem atrophy
  • shy-drager syndrome
  • olivopontocerebellar atrophy
  • wilson disease
  • multiple strokes
  • subdural hematoma
  • normal pressure hydrocephalus
  • basal ganglion lesion
  • hypothyroidism and hyperparathyroidism
  • post encephalitis
  • creutzfeldt jacob disease
77
Q

Tx of parkinson’s disease?

A
  • initial drug tx: carbidopa/levodopa (sinemet) or dopamine agonists - after 2-5 yrs levodopa becomes less effective
  • drugs that cause or worsen parkinsonism should be d/c
  • other options:
    Monoamine oxidase type B inhibitors
    catechol-methyltransferase inhibitors
    DBS: for drug resistant tremor or levodopa induced motor complications
  • tx best managed by multidisciplinary team, PT, OT, assistive devices, and measures to prevent falls
  • constipation common: prevented or relieved w/ dietary fiber, fruit juices, sometimes laxatives
  • a regular exercise program
78
Q

End of life issues for parkinson pts?

A
  • many pts eventually become severely impaired and immobile and are at risk for aspiration
  • eating may become impossible
  • dementia
  • discuss end of life care issues early
  • advise pt to appoint a surrogate to make medical care decisions if they become incapacitated
79
Q

What is polymyalgia rheumatica? Relationship w/ GCA?

A
  • inflammatory condition which is characterized by severe bilateral pain and morning stiffness of the shoulder, neck and pelvic girdle
  • there is some controversy as to whether or not PMR represents a form of GCA, however balance of evidence would appear to suggest 2 are distinct and relatively common diseases which often co-exist and which share many common features
80
Q

Epidemiology of PMR?

A
  • common condition of older age. It is rare under age of 50, but incidence rises w/ age w/ a peak b/t 70-80
  • incidence of disease in pts over 50 is about 100/10000
  • there is increased incidence of disorder at higher latitudes
  • women are more frequently affected than men w/ M:F ratio of 1:3
81
Q

Etiology of PMR?

A
  • still unknown, but has modest famial aggregation, linked to HLA-DRBI 04 and 01 alleles, which suggests genetic predisposition to enviro factors may play a part
  • viral or infectious cause has also been suspected due to increased prevalence of abs to RSV and adenovirus in PMR and assoc b/t the increased incidence of the disorder an d epidemics of mycoplasma pneumoniae, chlamydia pneumoniae and parvovirus B19
82
Q

Presentation of PMR?

A
  • may present w/ variety of signs and sxs howevere MC presenting sxs include bilateral severe, persistent pain in neck, shoulders, and pelvic girdle
  • other sxs and signs may include:
    pain on active and passive movement of jts (shoulder 70-95%, hips and neck 50-70%)
    morning stiffness of more than 1 hr and also after periods of rest
    myositis
    lethargy
  • loss of wt
  • depression
  • fever
  • jt effusions: asymmetric peripheral arthritis - mainly knee and wrist - carpal tunnel syndrome, edema of hands, wrist, ankles and feet
83
Q

DDx for PMR?

A
  • EORA (elderly onset RA)
  • SLE
  • Polymyositis
  • spondyloarthropathy
  • bacterial endocarditis
  • myeloma
  • paraneoplastic syndromes
  • primary systemic amyloidosis
84
Q

Labs for PMR?

A
  • ESR: most useful - raised to at least 40 mm/hr and often 100 mm/hr - although up to 20% of pts may have a normal ESR at dx - plasma viscosity can be used instead of ESR
  • CRP
  • IL-6 usually raised, and a useful marker of disease activity
  • CBC: normochromic, normocytic anemia (anemia of chronic disease)
  • rheumatoid and ANA not elevated
  • LFTs mildly elevated in 1/3 of pts
85
Q

Assoc disease of PMR?

A
  • GCA - co-exists in about 30% of pts w/ PMR and shares many features of the disease
86
Q

Management of PMR?

A
  • document sxs and level of any disability at dx
  • consider GCA in all people w/ PMR
  • advise people w/ PMR to seek medical attention if they developed any sxs of GCA - any new HA, jaw claudication or visual disturbances
  • monitor response to tx by assessing changes in clinical features and inflammatory markers: ESR/CRP
  • manage any residual physical or psychosocial disability caused by the disease
  • consider other possible dxs: particularly if sxs are not responding to tx
  • prednisone DOC - produces dramatic response, 18-24 months on tx usually, may need further tx for exacerbations
  • bisphosphonates, or Ca and Vit D - should be given to all pts who are receiving prednisone for more than 6 months
87
Q

Non-drug managemnt for PMR?

A
  • frequently elderly and may have mobility problems and difficulty w/ many aspects of daily living. Many pts will benefit from referral to a physiotherapist and OT for assessment
88
Q

Prognosis of PMR?

A
  • usually responds well to tx w/ steroids resulting in remission in majority of cases
  • relapse may occur, usually w/in 2 yrs of stopping steroids, but condition remains steroid responsive
  • morbidity and mortality may occur as a result of immunosuppression or steroid SEs, and pts should be regularly monitored while on steroids
89
Q

Cardinal sxs of PMR?

A
  • shoulder and hip girdle pain w/ pronounced stiffness lasting at least one hour
90
Q

Mimics of PMR?

A
  • infection, malignancy, metabolic bone disease, elderly onset RA

Geriatrics (16 decks)

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