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HTN & DM: Keara D. Acevedo, PTRP
HTN & DM: Keara D. Acevedo, PTRP
HTN & DM: Keara D. Acevedo, PTRP
• Types:
o Labile/Borderline: Intermittent elevation of BP interspersed
c N readings
o Masked Htn: N in clinic, high @ home
o White Coat Htn: elevated BP in clinic, N outside clinic
HYPERTENSION
• Factors that contributes to Htn:
o >20 y.o. = high BP
o 45 y.o. = M>F
45-64 y.o. = M=F
>65 y.o. = M<F
o Race: African American > Caucasian
o Heredity
o Pregnancy
HYPERTENSION
• Factors that contributes to Htn:
o Lifestyle
➢ Sedentary
➢ Smoking
➢ Heavy Alcohol Consumption
o Activity level
o Obesity
o Diet: High sodium intake
o Comorbidities – Cardiac & Vascular
o Meds: Steroids, NSAIDs, Diet Pills, Cyclosporine, Erythropoietin,
Tricyclic Anti-depressants, MonoAmine Oxidase Inhibitors, Oral
Contraceptives
HYPERTENSION
Factors Causing Increased BP
1. CO: Increased amounts of blood pumped into arteries → Arterial walls
distend --. Higher BP
2. Age:
• Normally rises gradually p birth; Peak @ puberty
• Late adolescence (18-19 y.o.) = adult BP (<120/<80 mmHg)
• 120/80 is PREHYPERTENSION; but is NOT A DISEASE category; A
risk factor for Htn identification
3. Exercise
• Physical Activities → Inc CO → Inc BP (Greater inc in SBP)
• BP increase is proportional to intensity of workload
• 10mmHg drop of SBP → STOP EXERCISE
HYPERTENSION
Factors Causing Increased BP
4. Valsalva Maneuver
• An attempt to exhale forcibly c glottis, nose & mouth closed
• Causes inc intrathoracic pressure c vein collapse of chest wall
• Dec in bf to heart → Dec Venous Return → Drop in BP → Release of
breath → Dec IntraThoracic Pressure → Venous Return is
reestablished (“Overshoot”) → Marked inc in HR & BP →
Bradycardia (vagal slowing of HR)
• Must be avoided by people c Heart dse & Htn
• May result in seeing “black dots” and feeling of dizziness
HYPERTENSION
Factors Causing Increased BP
5. Arm Position
• BP may vary as much as 20 mmHg by altering arm position
• Pt should be sitting c arm in horizontal supported position @
HEART LEVEL
HYPERTENSION
Anti-Hypertensive Drugs
Medication MOA Action Example SE
Diuretics “Water Pills” Inhibits reabsorption of Dec peripheral vascular Thiazide
water in kidneys resistance Furosemide (Lasix)
Bumex
Beta-Blockers Beta 1: Inc Heart Cxn “olols”
Beta 2: Bronchioles Relaxation
Non-Selective Beta- Inhibits (B) Beta 1 & 2 Propanolol CI in COPD
Blockers Nadolol
Penbutolol
Selective Beta Blockers Inhibits Beta 1 Atenolol
Metaprolol
Beta Agonist Stimulates Beta 1 & 2 Asthma Px Palpitations
For relaxation of
Bronchioles
HYPERTENSION
Anti-Hypertensive Drugs
Medication MOA Action Example SE
Ca Channel Blockers Inihibits the influx of Ca Dec HR “dipine”
in myocardium Vasodilation Amlodipine
Felodipine
Nisoldipine
Verapamil
Alpha-1 Blocker Alpha 1: Inhibits “zocin” Dizziness
Vasoconstriction Vasocontraction Terazocin Postural Hypotension
Alpha 2: Vasodilation Promotes Vasodilation Prazocin
Dexazocin
DIABETES MELLITUS
• Chronic disorder caused by deficient insulin or
defective insulin in the body
• Characterized by HYPERGLYCEMIA and disruption of
the metabolism of carbohydrate, fat and protein
• Main organ involved: PANCREAS
o “GABIDS”: Glucagon = Alpha Cell
Beta Cell = Insulin
Delta Cell = Somatostatin
DIABETES MELLITUS
• s/sx:
o Hyperglycemia, Glycosuria, Ketonuria
o 3 Ps (Polyuria, Polydipsia, Polyphagia)
o Unexplained Wt Loss
o Fatigue
o Blurred Vision, h/a
DIABETES MELLITUS
FACTORS TYPE 1 TYPE 2
Age of Onset < 30 y.o. >35 y.o.
Type of Onset Abrupt Gradual
Insulin Production Little-to-None Below/Above Normal
Incidence 5% - 10% 90% -95%
KetoAcidosis May Pccurs Unlikely
Insulin Injections Requires 20% - 30% of clients only
Body Weight Normal-toThin 80% obese
Management Diet, Exercise, Insulin Diet, insulin, oral hypoglycemics,
exercise
Etiology AutoImmune, Viral Obesity assoc to insulin receptor
resistance
Hereditary Yes Yes
DIABETES MELLITUS:
• TYPE I DM = Insulin-Dependent DM
o AutoImmune Dse (inhibits Beta Cell, no
release of Insulin)
o (-) Insulin
o New Source of ATP: tryglycerides → Ketone
Acid → Atherosclerosis
o Ectomorph (d/t Triglycerides)
o “Ketone Prone DM”
DIABETES MELLITUS:
• TYPE II DM = Non-Insulin Dependent DM
o Dec Insulin Production/Dec Insulin Receptors
sensitivity
o Obese
o Mx: diet/exercise
o “Ketone Resistant DM”
DIABETES MELLITUS RFs:
• Obesity (non-obese c inc body fat
% in Abdominal Region)
• Family Hx of Diabetes
• Unhealthy eating patterns
• Lack of Physical Activity
DIABETES MELLITUS RFs:
Abdominal
Triglycerides Low HDL
Obesity
1.Diet
2.Exercise
3.Medication
DIABETES MELLITUS
Insulin Reaction Time: