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
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
3
Q
How common is HTN in people older than 80?
A
- 65%
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
5
Q
What are assoc conditions of HTN?
A
- MI
- CVA
- PVD
- CHF
- Renal Failure
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
7
Q
What is preHTN?
A
- SBP: 120-139
or - DBP: 80-89
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)
9
Q
Dementia relationship w/ HTN?
A
- cognitive impairment more common w/ HTN
- reduced progression of dementia occurs w/ effective antiHTN therapy
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
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)
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
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
14
Q
Lab tests for HTN?
A
always: EKG UA Chem fasting lipid panel H/H, TSH
optional:
microalbumin
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
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
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
18
Q
What could a lack of BP drop of 10-20% during the night indicate?
A
- possible increased risk for CV events
19
Q
What home BP measurement is considered HTN?
A
- over 135/85
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
21
Q
Initial therapy for HTN w/ heart failure?
A
THIAZ, BB, ACEI, ARB, ALDO ANT
22
Q
Initial therapy for HTN w/ S/P MI?
A
- BB, ACEI, ALDO ANT
23
Q
Initial therapy for HTN w/ high risk of CAD?
A
- THIAZ, BB, ACEI, CCB
24
Q
Initial therapy for HTN w/ diabetes?
A
- THIAZ, BB, ACEI, ARB, CCB
25
Q
Initial therapy for chronic renal disease and HTN?
A
- ACEI and ARB
26
Q
Initial therapy for recurrent stroke prevention in pt w/ HTN?
A
- THIAZ, ACEI
27
Q
What other diseases are thiazides therapeutic for?
A
- osteopenia/osteoporosis
28
Q
Other uses for BBs?
A
- atrial tachycardias, migraine, thyrotoxocosis, essential tremor, perioperative period, peformance anxiety
29
Q
Other use for CCBs?
A
- raynauds
30
Q
Other use for Alpha-blockers?
A
- useful in BPH
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
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
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
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
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
36
Q
When would BP reading be falsely elevated in elderly pts?
A
- if they have really stiff, calcified arteries - known as pseudoHTN
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
