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ILE > Unit 1: Hypertension And Hypersensitivity > Flashcards

Unit 1: Hypertension And Hypersensitivity Flashcards

1
Q

What are sources of patient information?

A

Chief complaint, history of present illness, past medical history,past surgical history, social history, family history, medical history, allergies/intolerances, immunization history

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2
Q

Describe the purpose of a SOAP note.

A

SOAP notes are important because they are a part of the collecting process of the patient care process.

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3
Q

List the sections of a soap note.

A

Subjective, Objective, Assessment, Plan

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4
Q

Define subjective information

A

Subjection information is information provided to you by the patient during an encounter

Examples: chief complaints or reason for the visits, HPI (history of present illness)

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5
Q

Define objective information

A

Objective information is the physical findings and measurable/confirmable data relevant to the encounter

Example: medications, vitals, PE, labs, EHR data

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6
Q

Subjective or objective?

A blood pressure reading of 143/78 taken by the nurse in clinic.

A

Objective

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7
Q

Subjective or objective?

Glucose of 101 reported in the clinic.

A

Objective

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8
Q

Subjective or objective?

Patient medication list in patient handwriting.

A

Subjective

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9
Q

Subjective or objective?
Home BP readings in the patients BP log averaging around 130/80.

What is they bring in the monitor and the nurse can check the history on it?

A

Subjective

Objective

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10
Q

What is the proper technique for blood pressure measurement?

A

First- make sure the patient is in a seated position with their legs uncrossed and their arm is resting on a table or in a comfortable position.

Secondly- palpate the brachial artery and place the correct size cuff on the patient’s arm. (If the cuff is incorrect, replace with the correct size)

Finally- ask the patient what their normal BP is and inflate the cuff to about 20mmHg above their reported BP. Place the diaphragm of the stethoscope over the brachial artery. Listen for the beginning sounds and the ending sounds.

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11
Q

What essential components of a blood pressure measurement should be accurately reported?

A

In addition to the actual BP values and units:

The arm used for the measurement, the position of the patient, the cuff sized used,

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12
Q

What type of hypertension is has a definite cause for elevated BP, but the specific cause is not known?

A

Primary hypertension

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13
Q

What type of hypertension is caused by another medical condition?

A

Secondary hypertension

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14
Q

What is the classification for a BP that is <120mmHg systolic AND <80mmHg diastolic?

A

Normal BP

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15
Q

What is the classification for BP that is 120-129mmHg systolic AND <80mmHg diastolic ?

A

Elevated BP

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16
Q

What is the BP classification for 130-139mmHg systolic OR 80-89mmHg diastolic ?

A

Stage 1 hypertension

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17
Q

What is the BP classification of a BP that is >140mmHg systolic OR >90mmHg diastolic?

A

Stage 2 hypertension

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18
Q

What are some risk factors that can elevate BP?

What are some risk factors that are modifiable?

A

Family history, age, gender, race, chronic kidney disease

Lack of physical activity, an unhealthy diet, especially one high in sodium, being overweight or obese, sleep apnea, high cholesterol, diabetes, smoking and tobacco use, stress

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19
Q

What is masked hypertension?

A

Elevated blood pressure occurs outside of a medical environment (LVMI, smokers, drinkers, diabetics, hypertensive patients)

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20
Q

What is white coat hypertension?

A

Elevated blood pressure only occurs in a medical environment

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21
Q

What is the blood pressure goal for adult patients that are being treated for hypertension?

A

130/80mmHg

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22
Q

What is an adverse drug event?

A

An injury resulting from medical intervention related to a drug including medication errors, adverse drug reactions (ADR), allergic reactions, and overdoses

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23
Q

What is an ADR?

A

Undesirable effect of a medication caused by appropriate use of drug

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24
Q

All AD—s are AD—s but not all AD—s are AD—s

A

All ADRs are ADEs but not all ADEs are ADRs

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25
What are some symptoms associated with hypotension?
Dizziness or lightheaded ness, fainting (syncope), blurred vision, nausea, fatigue, lack of concentration
26
What BP thresholds classify hypotension?
<90mmHg systolic OR <60mmHg diastolic
27
How is hypertension diagnosed?
An average of 2 or more BP measurements are above the elevated threshold classification on more than one day.
28
Why is out-of-office monitoring of BP important?
Because it can rule out white coat hypertension. If the patient’s at home readings are just as high as they are while they are comfortable in their homes, then the doctor has a confirmed diagnosis
29
What are some of the long term complications associated with hypertension?
1. Heart attack/stroke/peripheral arterial disease (atherosclerotic cardiovascular disease (ASCVD)) 2. aneurysm 3. heart failure 4. chronic kidney disease 5. memory problems/dementia 6. thickened or torn or broken vessels in the eye
30
What drug class works to block the sodium chloride symporter in the distal convoluted tubule?
Thiazide diuretics
31
What four classes of drugs are considered first line anti hypertensives?
Thiazide diuretics Calcium channel blockers Angiotensin converting enzyme inhibitors (ACEI) Angiotensin (2) receptor blockers (ARBs)
32
Which of the two first line drug classes can you not use together? Why not
ACE inhibitors and ARBs. Because they both work to prevent angiotensin 2 from being able to produce aldosterone. They both increase potassium levels and decrease GFR Angiotensin 2 is important in maintaining normal flow through the glomerulus
33
What are some drugs within the thiazide class?
Hydrochlorothiazide and chlorthalidone
34
Describe the mechanism of action for thiazide diuretics What does this affect short term and long term?
They work to block the Na+/Cl- symporter. This reduces blood volume because Na is staying within the lumen to be excreted and is not being reabsorbed. Usually water would osmotically follow Na but since it is not being reabsorbed, neither is water. Short term: blood volume Long term: vascular resistance is reduced Long term vasodilation bc Na normally works as a vasoconstrictor in the vasculature but when it isn’t present, vasodilation occurs
35
Thiazide diuretics work to Increase excretion of: Decrease excretion of: What else?
Increase excretion of h20, Na+, K+, Mg+, Cl- Decrease excretion of Uric acid and Ca+ (may cause a gout attach in someone more prone to gout) Also may increase glucose levels
36
What are the two sub-classes of CCBs? What are drug examples of each?
Dihydropyridines (DHP) and Non-Dihydropyridines (Non-DHP) DHP - Amlodipine and other drugs ending in -dipine Non-DHP - Diltiazem and Verapamil (these are the only two drugs in this class)
37
What is the mechanism of action for bothering DHPs and Non-DHPs?
DHPs block the influx of Ca+2 into vascular muscle | Non-DHPs block Ca+2 entry into cardiac muscle
38
What are the adverse effects of CCBs? What do DHPs additionally effect? Why does this happen?
Hypotension, constipation, muscle weakness, flushing, swelling in the lower extremities, gingival hyperplasia, headache DHPs additionally may cause reflux tachycardia. This happens bc DHPs work only in the muscles of the vasculature so, the stretch receptors in the carotid artery sense the BP drop when a DHP is administered and triggers the brain the have a reflex response. The brain stimulates the sympathetic system to release epi from the CNS to try to “fix” the drop in BP by increasing the heart rate
39
What is the ending for ACE Inhibitors? And some drug examples
-pril Captopril, enalopril maleate
40
Discuss the mode of action of ACE inhibitors
They block the conversion of Angiotensin 1 to angiotensin 2 and blocks the breakdown of bradykinin. Angiotensin 2 is responsible for maintaining normal flow through the glomerulus, causing vasoconstriction, and for producing aldosterone which is important for Na retention (increasing blood volume thus increasing blood pressure) and K+ excretion due to the exchanger Bradykinin is a vasoconstrictor- ACEI block bradykinin from being broken down so the vasculature dilates Bradykinin inhibition increases cough and angioedema
41
What are some adverse effects of ACE | Inhibitors?
Hypotension, cough, increased K+ levels, angioedema, decreased GFR, rash, taste disturbances
42
What is the ending for ARBs? Drug examples?
-artan ending Valsartan
43
What are ARBs mode of action?
Antagonist of angiotensin 2 at angiotensin 1 receptors
44
What are the adverse effects of ARBs?
Hypotension, dizziness, headache, nausea and vomiting, cough, increased K+ levels, decreased GFR
45
Why is cough associated with ACE and ARBs but not as much with ARBs?
Because ARBs can still break down bradykinin
46
What are the normal lab values for Na+, K+, SCr, and glucose?
Na+ 136-145mEq/L K+ 3.5-5.0mEq/L Glucose 70-110mg/dL SCr 0.7-1.5mg/dL
47
What are the six classes of alternative antihypertensives?
``` Beta blockers Centrally acting antihypertensives Loop diuretics Aldosterone antagonists Alpha-1 antagonist Direct vasodilators ```
48
Which alternative drug is the first choice?
Beta blockers
49
What is the ending of beta blockers and drug examples?
-prolol | Metoprolol
50
What is the mode of action for beta blockers?
Decrease heart rate, decreased central sympathetic outflow, decreased renin release Decreased HR leads to a decrease in blood pressure bc it is working by blocking the Beta receptors on the heart Decreased sympathetic outflow by blocking it within the brain so the body will not respond by trying to raise BP Decreased renin release will slow the conversion of angiotensin 1 to angiotensin 2 preventing vasoconstriction to a certain degree
51
What are adverse effects associated with beta blockers ?
Bradycardia, sedation, fatigue, shortness of breath (SOB), headache, sleep disturbances, sexual dysfunction
52
What drug class is clonidine a part of?
Centrally acting antihypertensives
53
What is the modes of action for centrally acting antihypertensives?
Decreased sympathetic outflow, several are alpha-2 agonists Alpha-2 agonists work to shut down further release of neurotransmitter.... alpha-2 agonist prevents the release of norepi A few alpha-2 receptors are in the vasculature and mediate vasoconstriction but are soon overcome bc clonidine gets into the CNS rapidly
54
Sedation, bradycardia, constipation, dry mouth, and dizziness are all adverse effects of which antihypertensive drug class?
Centrally acting antihypertensives
55
What kind of antihypertensive is lasix (furosemide)?
Loop diuretic
56
What is the mode of action for loop diuretics?
They are the most powerful diuretics known due to their site of action. Inhibition of the Na+/K+/2Cl- symporter results in a powerful diuretic effect resulting in the loss of these ions along with Ca+2 (retained with thiazide diuretics) and Mg+2 (used when blood volume is high)
57
Why are thiazide diuretics used over loop diuretics?
Because thiazide reduce the overall risk of cardiovascular disease, they are a first line agent, and they are used in patients who don’t have a lot of calcium in their diet. Loop diuretics result in a loss of Ca too
58
What is the adverse effect of loop diuretics.
Electrolyte embalance
59
Spironolactone and eplerenone are examples of what drug class?
Aldosterone antagonists
60
Aldosterone antagonists are considering as what type of diuretic ?
K+ sparing
61
What are in the mode of action for aldosterone antagonists?
Inhibits aldosterone mediated stimulation of ENaC and Na+ATPase synthesis resulting in increased Na+ excretion and decreased K+ excretion
62
What are adverse effects of aldosterone antagonists?
N/V, headache, rash and hyperkalemia, Spironolactone is also a potent anti-androgenic (partial agonist) compound and may produce gynecomastia, impotence, and menstrual disorders
63
What ending is denoted for alpha-1 antagonist drugs? What are some examples?
-sin | Terazosin
64
Discuss alpha-1 antagonist mode of action
Blocks alpha-1 receptors in the vasculature to promote vasodilation
65
Adverse effects of alpha-1 antagonists are
Hypotension, fainting, N/V, runny nose, sexual dysfunction (happens when you inhibit adrenergic function)
66
What are some examples of direct vasodilators?
Hydralazine and minoxidil
67
What is the mode of action of direct vasodilators?
Open potassium channels resulting in hyper polarization of vascular smooth muscle
68
What are the adverse effects of direct vasodilators?
Hypotension, reflex response, hypertrichosis (hair growth)

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