M1 recap Flashcards

1
Q

types of pain

acute,
chronic
intractable
neuropathic

A

Acute Pain:
- pain directly related to tissue injury, resolves when tissue heals

Chronic (Persistent) Pain:
- pain that persists beyond three months secondary to chronic disorders, or damaged nerves after healing is complete

Intractable Pain:
- A pain state that is usually severe in which there is no cure, after accepted medical treatments have been offered (i.e. Refractory Angina)

Neuropathic Pain:
- Pain that is related to malfunctioning or damaged nervous tissue
- Shingles, fibro

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2
Q

types of pain

nociceptive
somatic
visceral
pain threshold
phantom pain

A

Nociceptive
- caused by damage to somatic or visceral tissue

Somatic
- localized to areas such as bone, joint, muscle or skin
- Aching or throbbing


Visceral
- activation of nociceptors of the thoracic, pelvic, or abdominal viscera (organs).

Pain Threshold:
- The process of recognizing, defining, and responding to pain

Phantom Pain:
- Painful sensations experienced from a limb that has been removed (amputated)

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3
Q

Meds for scale of pain (1-10)

A

Medication for mild pain (1-3)
NSAIDs
nonopioid analgesics
Tylenol → acetaminophen
Advil → ibuprofen

Mild to moderate pain (4-6)
prescriptions for opioids are often combined with a nonopioid analgesic (tylenol 3 EG)

Moderate to severe pain (6-10)
Morphine is one of the opioids most commonly prescribed for moderate to severe pain, although fentanyl (Duragesic), hydromorphone (Dilaudid), methadone (Metadol), and oxycodone also are used extensively.

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4
Q

lung capacity

TV,IRV,ERV,VC

A

Lung Capacity (important)
- Tidal volume (TV or VT): air volume of each breath (500ml)

Inspiratory reserve volume (IRV):
- maximum volume that can be inhaled after a normal inhalation

Expiratory reserve volume (ERV):
- maximum volume exhaled after a normal exhalation

Vital capacity (VC):
- the maximum volume of air exhaled from a maximal inspiration, VC = TV + IRV + ERV (average is 6L)

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5
Q

restrictive vs obstructive PD

what causes a restictive PD

A

issue with Inflow of air
Decreased lung compliance and decreased lung expansion
Problem of volume rather than airflow (speed)

Caused by:
Decreased number of functioning alveoli
Lung tissue loss (lobectomy/tumour)
Hypoxemia – low oxygen in blood
Hypoxia – low oxygen in tissue

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6
Q

RPD

pneumonia

what is it? some S/S

A

Inflammation of lung tissue

Classic Signs and Symptoms
- Tachypnea
- Productive cough
- Fever
- Dyspnea
- Crackles, decreased breath sounds
- ABGs indicative of hypoxemia (o2 level and Co2 level)

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7
Q

RPD

classifications of Pneumonia

A

Classification often based on where acquired
- Ventilator-associated pneumonia (VAP)
- Health care-associated pneumonia (HCAP)
- Community AP: Streptococcus pneumoniae (gram +ve)
- Hospital AP: Pseudomonas (gram –ve, opportunistic)

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8
Q

Anti-infective tx

A

Penicillins (Oxacillin, Antipseudomonal)
Tetracyclines
Aminoglycosides
Cephalosporins (Ceftriaxone)
Macrolides (Clarithromycin)
Fluoroquinolones (Ciprofloxacin)

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9
Q

RPD

bronchitis

A

Chronic sputum production with a cough on a daily basis for a minimum of 3 months/year

Chronic hypoxemia/cor pulmonale (right sided HF)
Increased mucus production
Increased bronchial wall thickness (obstructs air flow)
Increased CO2 retention/acidemia
Reduced responsiveness (hypoxemia)

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10
Q

RPD

emphysema

A

Abnormal enlargement of the air spaces distal to the terminal alveolar walls

S/S
- Barrel chest // thin due to energy required to breathe
- dyspnea
- decreased gas exchange surface area
- Decreased capillary network
- increased O2 consumption

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11
Q

obstructive PD

A

Air flows readily into lungs, trapping occurs in aveoli
Causes prolonged expiratory phase
CO2 can get trapped if alveoli not empty prior to inhalation
hyperinflation with poor elastic recoil

Examples:
Asthma
status asthmaticuz
COPD
CF

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12
Q

OPD

status asthmaticus

what is it? physiological changes that occur? S/S

A

Life threatening due to airway obstruction

Physiologic Changes:
- Inflammation causing narrowing/ remodelling of the airway
- Hyper-responsiveness to irritants: bronchospasms and mucous plugging

Symptoms of Status Asthmaticus
- Pulsus paradixus of 25mm Hg or greater
- ABG showing hypoxemia with or without hypercapnia (++CO2)
- Reduced peak expiratory flow rate (30% or less of predicted value)
- dyspnea (Inability to speak or only 1 word phrases)

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13
Q

COPD

What is it? some causes?surgery? pharm?

A

resp disorder causing airflow limitation, associated with a chronic inflammatory response in the airways and the lung. (caused largely by smoking )

Surgery
lung volume reduction surgery
lung transplantation

pharm
- B2 Adremergic agonist (inhaled short acting or long acting)
- corticosteroids

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14
Q

OPD

TB

pharm

A

TB is caused by the Mycobacterium tuberculosis or the tubercle bacillus, an acid-fast organism, spread by airborne transmission.


pharm
- Isoniazid
- Pyridoxine
- Rifampin
- Pyrazinamide

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15
Q

OPD

CF

A

An autosomal recessive, cuased by altered function of the exocrine glands involving primarily the lungs, pancreas, and sweat glands

Abnormally thick, abundant secretions from mucous glands lead to a chronic, diffuse, obstructive pulmonary disorder in almost all patients.

Chronic fatal respiratory disease
The most common genetic disease

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16
Q

pneumothorax

A

Presence of air in the pleural space

Types of pneumothorax
Closed pneumothorax
Open pneumothorax
Tension pneumothorax
Hemothorax

Small: mild tachycardia and dyspnea
Large: respiratory distress, shallow, rapid respirations; dyspnea; decreased O saturation

17
Q

CO, heart rate, stroke volume, pulse pressure and mean arterial pressure

A

Cardiac output (CO) = blood pumped/min
Normal 4-8L/min

Heart rate (HR)
Stimulation from SNS
Stimulation from PNS

Stroke volume (SV) = beat
SV = CO/HR

Pulse pressure (40 mmHg)
Differences between SBP and DBP
Normally 1/3 of SBP

Mean Arterial Pressure (MAP)
MAP = SBP + 2(DBP) / 3
Indicator of blood flow (better than SBP)
MAP >60 needed to maintain adequate tissue perfusion

18
Q

preload

A

Volume of blood in ventricles at end of diastole
Affected by the amount of blood delivered to the heart

Conditions that diminish preload:
- Decreased blood volume
- AV valve dysfunction
- Vasodilation

Conditions that increase preload
- Increase blood volume
- Poor EF/CHF- inability to eject

19
Q

afterload

what causes increased/decreased afterload, impact on CO?

A

The peripheral resistance against which the left ventricle must pump

increased afterload
- vasoconstriction, hypertension

decreased afterload
- vasodilation, shock\

Impact of afterload on CO
If afterload ↑, CO ↓, arterial pressure ↑
If afterload ↓, CO ↑, arterial pressure ↓

20
Q

contractility (EF)

what increases/ decreases

A

The heart’s ability to function as a pump

Conditions that affect contractility
↑ vasoconstriction
- calcium release, dopamine, doubutamine

↓ contractility:
HYPOXIA ischemia and drugs (narcotics, anesthetics)

21
Q

hypertesive medications

A

Diuretics (Furosemide, HCTZ)
Antihypertensives (ACE Inhibitors, Calcium Chanel blockers)
beta blockers

22
Q

CAD

what is it? what causes it? some medications used?

A

CAD results in ischemia and infarction of myocardial tissue.
LAD (left anterior descending artery) is most commonly affected.
Highly sensitive CRP (risk of MI)

some causes:
- Atherosclerosis
- Coronary vasospasm
- Microvascular angina

medication therapies;
- morphine
- B-blockers
- Calcium channel blockers
- Nitrates
- Thrombolytics
- Cholesterol-lowering medication therapy
- Antiplatelet therapy

23
Q

valve regurgitation

mitral and aortic

A

Mitral valve regurgitation (MR)
- Insufficient or incompetent mitral valve (prolapse)
- Regurgitation of blood back into LA
- Can lead to left sided heart failure

Aortic valve regurgitation (AR) – aka aortic insufficiency
- Incompetent aortic valve, allows blood from aorta back into LV during diastole
- LV hypertrophy to maintain Stroke Volume

24
Q

LSHF

causes? signs? findings?

A

Causes:
- LV infarct, cardiomyopathy, hypertension


Signs:
- S3 gallop, tachycardia
- inspiratory rales beginning at lung bases
- expiratory wheezes due to bronchospasms

findings:
- hypoxemia
- pulmonary edema or pleural effusions

25
Q

RSHF

A

Causes:
- LHF
- RV infarct
- pulmonary or tricuspid valve disease,
- pulmonary HTN
- Pulmonary Edema

Systemic Congestion

Signs:
- hepatomegaly ascites
- peripheral or sacral edema
- pleural and pericardial effusions

Lab Tests:
- ↑ LFTs, ↑BUN/Cr, ↑ PT/INR,
- hyponatremia

26
Q

HF medications

A

Medications
- ACE Inhibitors
- ARBs (angiotensin blockers)
- Beta blockers
- Loop and Thiazide diuretics

(Fluid restrictions)

27
Q

angina

supply vs demands

A

Increased demands
- ↑ heart rate, ↑ contractility, ↑ preload

Decreased supply
- CAD, spasm, anemia, hypoxemia, shock

28
Q

angina managment

A

nitrates
nitroglycerine
beta adrrenergic blockers
calcium channel blockers
ACE inhibitors

29
Q

unstable angina indications

A

Pain is increasing in severity; unrelieved w/ Ntg
Rest angina

Indicative of unstable plaque
Preinfarct or crescendo

30
Q

Hyperosmolar Hyperglycemic Syndrome (HHS)

A

Life-threatening syndrome
- Often occurs in patients older than 60 years
with type 2
- Patient has enough circulating insulin that
ketoacidosis does not occur
- Produces fewer symptoms in earlier stages
- Neurological manifestations occur because of ↑ serum osmolality

Laboratory values
 Blood glucose >34 mmol/L
 Increase in serum osmolality
 Absent/minimal ketone bodies

31
Q

nsg managment DKA/HHS

A

Nursing management DKA/HHS
- Patient closely monitored

Administration
- IV fluids
- Insulin therapy
- Electrolytes

Assessment
- Renal status
- Cardiopulmonary status
- Level of consciousness