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
Initial therapy for chronic renal disease and HTN?
- ACEI and ARB
26
Initial therapy for recurrent stroke prevention in pt w/ HTN?
- THIAZ, ACEI
27
What other diseases are thiazides therapeutic for?
- osteopenia/osteoporosis
28
Other uses for BBs?
- atrial tachycardias, migraine, thyrotoxocosis, essential tremor, perioperative period, peformance anxiety
29
Other use for CCBs?
- raynauds
30
Other use for Alpha-blockers?
- useful in BPH
31
Relative CIs for antiHTN drugs?
- 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
What is postural hypotension? When should orthostatics be checked?
- 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
What are HTN emergencies?
- 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
What are HTN urgencies?
- marked BP elevation but no acute TOD
- usually doesn't reqr hospitalization
- does reqr immediate combo oral antiHTN therapy
35
MC HTN in geri population? Cause of this?
- 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
When would BP reading be falsely elevated in elderly pts?
- if they have really stiff, calcified arteries - known as pseudoHTN
37
Tx of ISH when systolic is greater than 160 reduces incidence of what?
- MI, stroke and HF
38
in elderly - all cause mortality rates increase when DBPs are in what ranges?
- DBP: over 80
| - DBP: under 60
39
Goal for BP in elderly? What should you eval for?
- goal: under 140/90
- eval for:
target organ damage
other CV RFs
40
How common is cerebrovascular disease?
- 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
What are complications of a stroke?
- 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
Major RFs for a stroke?
- 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
Classification of a stroke?
- ischemic (75% of strokes - due to embolus or thrombosis)
| - hemorrhagic
44
What is a TIA?
- 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
What is a completed stroke?
- 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
MC blocked artery in a stroke?
-Middle cerebral artery
47
What does stroke presentation depend on?
- on affected vessel and whether or not there are any further complicating factors
48
Diff stroke syndromes (location of affected vessel)?
- ICA occlusion
- ACA occlusion
- MCA occlusion
- OCA occlusion
- verterbrobasilar occlusion
- lacunar infarct
- spinal stroke
49
Presentation of anterior circulation TIA/stroke?
- anterior or middle cerebral artery involved
- amaurosis fugax (monocular blindness)
- face-hand-arm-leg contralateral hemiparesis
- aphasia/dysarthria
50
Presentation of MCA occlusion?
- 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
Presentation of ACA occlusion?
- 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
Presentation of posterior TIA and stroke?
- vertigo
- diplopia/dysconjugate gaze, ocular palsy homonymous hemianopsia
- sensorimotor deficits - ipsilateral face and contralateral limbs, drop attack (rarely TIA)
- dysarthria
- ataxia
53
Presentation of vertebro-basilar posterior circulation occlusion?
- 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
Spinal stroke presentation?
- rare
- anterior spinal artery
- assoc w/ prolonged hypotension and intraspinal mass lesions
55
What is a lacunar infarct? Presentation?
- 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
Diff hemorrhagic strokes? Presentation?
- 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
Types of intracerebral hemorrhages?
- HTN atherosclerotic hemorrhage, lobar hemorrhages, hemorrhage from vascular malformations and uncommonly bleeding into brain tumors, blood dyscrasias or anticoag, and inflammatory vasculopathies
58
Cause of subarachnoid hemorrhage? How common?
- 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
signs and Sxs of subarachnoid hemorrhage?
- 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
DDx of a stroke?
- 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
Causes? Presentation of a intracerebral hemorrhage?
- 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
Dx of a stroke?
- 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
Management of an acute stroke?
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
Are anticoag indicated in acute setting of a stroke?
- no, recent studies have shown no short or long term benefit of admin heparin for acute ischemic stroke
65
Use of tPA for stroke?
- 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
CI to thrombolytics?
- 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
Acute or chronic prophylactic anti-platelet therapy?
- role of ASA (81 mg vs 325 mg)
| - Plavix (not Ticlodipine)
68
When is chronic proph. anticoag indicated?
- 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
Chronic management for pts who suffered a stroke?
- multidisciplinary approach
- psych services
- PT/OT/ speech language
- VNS/home health attendant
- skilled nursing facility
- social services
- family support groups
70
When is a carotid endartectomy indicated?
- 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
What is parkinson's disease? Characterized by?
- 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
What else may parkinson's pts develop? What else may cause this?
- dementia
| - similar sxs (called parkinsonism) may occur secondary to other disorders, drugs (esp antipsychotics) or toxins
73
Dx parkinson's?
- 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
Sxs reported by parkinson's pts?
- 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
Physical findings in parkinson's disease?
- 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
DDx for parkinson's?
- 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
Tx of parkinson's disease?
- 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
End of life issues for parkinson pts?
- 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
What is polymyalgia rheumatica? Relationship w/ GCA?
- 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
Epidemiology of PMR?
- 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
Etiology of PMR?
- 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
Presentation of PMR?
- 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
DDx for PMR?
- EORA (elderly onset RA)
- SLE
- Polymyositis
- spondyloarthropathy
- bacterial endocarditis
- myeloma
- paraneoplastic syndromes
- primary systemic amyloidosis
84
Labs for PMR?
- 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
Assoc disease of PMR?
- GCA - co-exists in about 30% of pts w/ PMR and shares many features of the disease
86
Management of PMR?
- 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
Non-drug managemnt for PMR?
- 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
Prognosis of PMR?
- 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
Cardinal sxs of PMR?
- shoulder and hip girdle pain w/ pronounced stiffness lasting at least one hour
90
Mimics of PMR?
- infection, malignancy, metabolic bone disease, elderly onset RA
