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Non-cardiovascular conditions (CMC) Flashcards

1
Q

The respiratory system plays a crucial role in maintaining homeostasis by

A

facilitating gas exchange, delivering oxygen to the bloodstream and expelling carbon dioxide from the body

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2
Q

name the structures of the respiratory system

A

divided into upper and lower respiratory tracts, including nasal cavity, pharynx, larynx, trachea, bronchi, and lungs

(trachea is start of lower, or the area below the vocal cords so part of the larynx? but basically trachea)

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3
Q

what is an acute PE?

A

sudden blockage in one of the pulmonary arteries in the lunges, typically caused by blood clots that travel to the lungs from other parts of the body, a condition known as DVT. This blockage can cause significant impairment in pulmonary circulation, leading to respiratory distress and potencial CV compromise.

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4
Q

describe the pathophys of acute PE

A

involves obstruction of blood flow, which increases PVR. this increased resistance puts strain on the RV of the hart, which has to work harder to pump blood through the obstructed pulmonary circuit. If untreated, this can lead to RV failure and decreased CO, potentially resulting in hemodynamic instability and shock

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5
Q

s/s of PE

A

variety. sudden SOB, pleuritic chest pain (sharp pain that worsens with breathing), hemoptysis, signs of right heart strain (JVD)

if severe: syncope, sudden CV collapse

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6
Q

dx of PE

A

CTPA: computed tomography pulmonary angiography to visualize presence of clots in pulm arteries
additionally: D-dimer blood test, which can indicate clot formation
echo: to assess RV function

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7
Q

PE management

A

focus is on stabilizing patient and preventing further clot formation

AC therapy (heparin, DOAC)
if contraindicated or insufficient, thrombolytic therapy may be used.

if massive or hemodynaic instability: embolectomy or catheter-directed therapies may be necessary

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8
Q

PE prevention

A

prophlyactic AC for high risk patients
mechanical methods: compression stockings
lifestyle modifications to reduce risk factors for DVT

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9
Q

What is ARF (acute respiratory failure)?

A

life threatening condition characterized by the inability of the respiratory system to maintain adequate gas exchange, resulting in hypoxemia and/or hypercapnia.

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10
Q

In ARF, primary dysfunction involves either a failure in

A

oxygenation or ventilation

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11
Q

Describe Type 1 respiratory failure

A

aka oxygenation failure.
marked by a PaO2 less than 60 mmHg with normal or low PaCO2.
commonly due to conditions like pneumonia, pulmonary edema, or ARDS, where there is impaired gas exchange at the alveolar level.

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12
Q

Describe Type 2 respiratory failure

A

aka ventilatory failure
presents with PaCO2 greater than 50mmHg and often associated with hypoxemia

causes include COPD, neuromuscular disorders, or CNS depression affecting respiratory drive

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13
Q

clinical presentation of ARF

A

dyspnea, tachypnea, cyanosis, AMS, use of accessory muscles
abnormal ABGs: indicating hypoxemia and or hypercapnia

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14
Q

management of ARF

A

treat underlying cause, support oxygenation and ventilation
-supplemental oxygen. in cases of ventilatory failure or severe hypoxemia unresponsive to oxygen therapy alone, may need mechanical ventilation

NIPPV can be used sometimes to avoid intubation

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15
Q

Pharm interventions for ARF

A

bronchodilators for bronchospasm
corticosteroids for inflammation
abx for infection
diuretics for fluid overload

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16
Q

What is ARDS (acute respiratory distress syndrome)?

A

severe, life-threatening condition characterized by the acute onset of widespread inflammation in the lungs. It can result in impaired gas exchange and can lead to significant respiratory fialure. Often seen in critically ill pts and can be triggered by various direct or indirect insults to the lunge, such as pneumonia, sepsis, trauma, or inhalation injury

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17
Q

describe pathophys of ARDS

A

marked by increased permeability of the alveolar-capillary barrier, leading to pulmonary edema that is not caused by cardiac failure. This results in reduced lung compliance and impaired oxygenation. The hallmark of ARDS is the rapid onset of severe dyspnea, hypoxemia, and bilateral infiltrates on chest imaging that cannot be attributed to heart failure or fluid overload.

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18
Q

the categories of ARDS are based on

A

degree of hypoxemia: mild, moderate, severe

determined by the PaO2/ FiO2 ratio while on PEEP of at least 5cm H2O

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19
Q

mild vs mod vs severe ARDS

A

mild: PaO2/ FiO2 ratio between 200-300mmHg
mod: between 100-200mmHg
severe: less than 100 mmHg

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20
Q

management of ARDS

A

supportive care with mechnical ventilation using lung-protective strategies.
-includes low TV ventilation (6ml/kg of predicted body weight) and maintaining plateau pressures below 30cm of H2O to prevent ventilatory-induced lung injury

prone positioning has been show to improve oxygenation and outcomes in severe cases

other: conservative fluid management to minimize pulmonary edema
tx of underlying causes
prevention of complications (DVT, stress ulcers)
Pharm has limited roles. NMB in early severe ARDS to improve oxygenation

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21
Q

What is acute lung injury?

A

critical condition characterized by acute and persistent lung inflammation, leading to increased pulmonary vascular permeability and non-cardiogenic pulmonary edema.

It is an intermediary state between normal lung function and ARDS, with ALI being a less severe form.

defined by the acute onset of hypoxema, AEB PaO2/ FiO2 of less than 300mmHg, bilateral infiltrates, and absense of left atrial HTN (which differentiates it from cardiogenic pulmonary edema)

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22
Q

pathophys of ALI

A

direct or indirect lung insults

direct: pneumonia, aspiration, inhalation injury

indirect: systemic inflammatory responses such as sepsis or pancreatitis

the resultant damage to the alveolar-capillary membrane increases its permeability, allowing protein-rich fluid to leak into the alveoli, impairing gas exchange

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23
Q

clinical presentation of ALI

A

acute onset dypsniea, tachypnea, refractory hypoxemia
crackles due to alveolar flooding
ABG- hypoxemia and resp alkalosis initially
bilateral infiltrates without evidence of LA HTN or significant pleural effusions

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24
Q

management of ALI

A

supporitve care. underlying cause.
mechanical ventilation with low TV to prevent further lung injury
PEEP is used to maintain alveolar recruitment and improve oxygenation.
fluid management to maintain adequate perfusion while avoiding overload

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25
what is the pleura/pleural cavity?
cavity: thin fluid-filled space between the two laters of the pleura surrounding the lungs. pleura: consists of two layers. Visceral pleura covers the lungs. Parietal pleura lines the chest wall. the pleural space contains a small amount of lubricating fluid to allow for smooth movement during respiration
26
what is a pleural effusion?
excessive accumulation of fluid within the pleural space.
27
what causes a pleural effusion?
can result from heart failure, infections (pneumona/tb), malignancies, or inflammatory diseases
28
s/s pleural effusion dx/ tx
dyspnea, CP, reduced breath sounds -CXR, US, thoracentesis
29
what is hemothorax?
accumulation of blood in pleural cavity, often due to trauma or surgical complications. presents with s/s of hypovolemic shock and respiratory distress. management: volume resuscitation and evac of blood via thoracostomy
30
what is chylothorax?
accumulation of lymphatic fluid (chyle) due to thoracic duct injury or obstruction. presents with milky pleural fluid upon thoracentesis and requires dietary modifications and possibly surgical intervention.
31
what is pneumothorax?
accumulation of air in pleural space, area between the lung and the chest wall, which can lead to partial or complete collapse of the affected lung. disrupts normal negative pressure that keeps the lungs inflated, resulting in impaired respiratory function.
32
types of pneumothorax
spontaneous (primary or secondary), traumatic, iatrogenic
33
how does primary pneumothorax typically occur?
usually in young, healthy individuals without apparent lung disease, often due to the rupture of small air blisters (blebs) on the lung surface
34
how does tension pneumothorax develop?
trapped air progressively accumulates under pressure, leading to mediastinal shift and CV compromise.
34
how does secondary pneumothorax typically occur?
in patients with underlying lung pathology, such as COPD, cystic fibrosis, or TB
35
dx of pneumothorax
imaging CXR to assess pleural space and lung collapse sometimes CT for more info on the extent and underlying cause
36
management of pneumothorax
depends on size and severity. some spontaneous larger/ symptomatic: needle aspiration or CT insertion to evacuate air from pleural space and re expand lung. Sx: video-assisted thoracoscopic surgery (VATS) for recurrent episodes.
37
what is pulmonary hypertension?
elevated blood pressure in pulmonary arteries, leading to increased resistance to blood flow through the lungs. defined by a mean PAP (mPAP) of 20mmHg or more at rest, measured by RHC.
38
causes of pHTN
genetic predisposition connective tissue diseases congenital heart defects certain drugs or toxins
39
classes of pHTN
1. pulmonary arterial hypertension 2. PH due to left heart disease 3. PH due to lung diseases and/or hypoxia 4. chronic thromboembolic PH (CTEPH) 5. PH with unclear multifactorial mechanisms
40
primary path of pHTN
vasoconstriction, vascular remodeling, thrombosis in situ within the small pulmonary arteries. leads to increases PVR and eventually right heart failure if left untreated
41
PH due to left heart disease is typically associated with conditions such as
heart failure with preserved or reduced EF, mitral valve disease, and other cardiac pathologies that increase left atrial pressure, subsequently elevated pressures in the pulmonary circulation
42
contributors of pHTN related to lung disease or hypoxia and generally why these are problematic
COPD interstitial lung disease sleep apnea living at high altitudes -resulting hypoxic vasoconstriction and structural changes in the pulmonary vasculature lead to increases pressures
43
how does CTEPH occur?
from unresolved pulmonary emboli that cause mechanical obstruction of the pulmonary vasculature, necessitating surgical intervention or targeted medical therapy for management
44
s/s pHTN
DOE, fatigue, CP, syncope, edema
45
dx pHTN
echo RHC PFTs CT or V/Q scans
46
management of pHTN
depend on underlying cause endothelin receptor antagonist phosphodiesterase-5 inhibitors prostacyclin analogs AC for CTEPH address comorbidities
47
what is sleep apnea?
sleep disorder characterized by repeated interruptions in breathing during sleep. can last from a few seconds to minutes and may occur multiple times per hour. excessive daytime sleepiness, loud snoring, observed apneas
48
most common form of sleep apnea
obstructive. occurs when muscles at back of throat relax excessively, causing airway blockage.
49
central sleep apnea
involves brain failing to send appropriate signals to muscles that control breathing.
50
why is sleep apnea significant in cardiac patients?
the repeated episodes of hypoxia and hypercapnia lead to SNS activation causing fluctuations in blood pressure and heart rate. can exacerbate current cardiac conditions such as HTN, HF, afib, CAD
51
pathophysiology of OSA
collapse of pharyngeal muscles during sleep, leading to partial or complete airway obstruction. results in decreased airflow despite continued respiratory effort. resulting hypoxemia triggers arousal from sleep to restore normal breathing, fragmenting sleep architecture and reducing restorative sleep stages.
52
dx of sleep apnea
polysomnography (comprehensive recording of biophysiological changes during sleep) measures parameters such as airflow, blood oxygen levels, heart rate, muscle activity an apnea-hypopnea index (AHI) is calculated to determine the severity of the condition
53
management sleep apnea
lifestyle mod (weight loss, positional therapy) CPAP (gold standard for OSA)
54
what is the endocrine system?
a complex network of glands and organs that produce, store, and secrete hormones. These hormones are chemical messengers that regulate various physiological processes, including metabolism, growth, development, tissue function, sexual function, reproduction, sleep, and mood.
55
hormones part of the stress response in the body
adrenaline (epinephrine) noradrenaline (norepinephrine) cortisol
56
the thyroid glands produce which hormones
thyroxine (T4) triiodothyronine (T3) impact HR, CO, SVR
57
hyperthryoidism can lead to
tachycardia, increased CO, afib
58
hypothyroidism can lead to
bradycardia, reduced CO
59
describe renin-angiotensin-aldosterone system
renin is produced by the kidneys, initiates cascade resulting in formation of angiotensin II. angiotensin II constricts blood vessels and stimulates aldosterone release from adrenal glands. aldosterone promotes sodium retention and potassium excretion, contributing to blood pressure regulation. dysregulation of RAAS can lead to HTN and HF.
60
ADH is released from
pituitary gland regulates water balance by controlling urine concentration in the kidneys. imbalances in ADH can affect blood volume and pressure.
61
list hormones the adrenal glands produce
cortisol aldosterone adrenaline noradrenaline
62
What is Addison's disease?
aka primary adrenal insufficiency occurs when the adrenal glands do not produce enough cortisol and aldosterone. s/s fatigue, muscle weakness, weight loss, low bp, hyperpigmentation of the skin
63
What is an Addisonian crises?
severe form of Addison's disease that can lead to shock and requires immediate medical attention
64
What is Cushing's syndrome?
excessive cortisol production. may be due to prolonged use of corticosteroids or tumors that produce adrenocorticotropic hormone (ACTH), leading to increased cortisol levels. s/s obesity with moon face, htn, DM, osteoporosis, skin changes such as bruising and striae
65
what is pheochromocytoma? dx?
adrenal disorder characterized by tumors in the adrenal medulla that cause overproduction of catecholamines (adrenaline and noradrenaline). leads to episodic or persistent HTN, palpitations, sweating, headaches, and anxiety. dx: biochemical tests for elevated catecholamine levels and imaging studies to locate the tumor
66
what is congenital adrenal hyperplasia (CAH)?
genetic disorder affecting cortisol synthesis due to enzyme deficiencies. results in excessive or deficient production of sex steroids or mineral corticosteroids. can lead to ambiguous genitalia in newborns and can affect growth and development if untreated.
67
what is diabetes mellitus?
chronic metabolic disorder characterized by hyperglycemia due to defects in insulin secretion, insulin action, or both. major risk factor for CV diseases, which are leading cause of morbidity and mortality among diabetic patients.
68
type 1 vs type 2 DM
1: autoimmune condition in which body's immune system attacks and destroys insulin-producing beta cells in the pancreas, leading to absolute insulin deficiency. commonly presents in childhood or adolescence but can occur at any age. 2: results from insulin resistance combined with relative insulin deficiency. often associated with obesity, sedentary lifestyle, and genetic predisposition.
69
how are diabetes and cardiac conditions related?
chronic hyperglycemia in diabetes leads to long-term damage and dysfunction of various organs, particularly heart and blood vessels. accelerates atherosclerosis, increasing risk of CAD, MI, stroke. diabetic cardiomyopathy (ventricular dysfunction independent of CAD or HTN, is another cardiac complication
70
diabetes management
lifestyle modification, pharmacotherapy, regular monitoring (hgb A1c). dietary adjustments and regular physical activity to enhance insulin sensitivity oral hypoglycemic agents like metformin or sulfonyureas for Type 2 insulin therapy both types when necessary
71
signs of poor glycemic control
polyuria polydipsia fatigue weight loss
72
acute complications of DM
DKA or HHS (hyperosmolar hyperglycemic state)
73
what is metabolic syndrome? criteria?
a cluster of interrelated risk factors that significantly increase likelihood of developing CV disease and T2DM. at least 3 of the following: -abdominal obesity -elevated triglycerides -reduced HDL cholesterol -HTN -impaired fasting glucose (each contribute to CV risk but coexistence amplifies risk)
74
how do high triglycerides and low HDL contribute to atherosclerosis?
elevated triglycerides are associated with increased production o very low density lipoprotein (VLDL) low HDL levels impair reverse cholesterol transport
75
how does metabolic syndrome predispose Indvidual's to diabetes and exacerbate endothelial dysfunction and atherogenesis
hypertension in metabolic syndrome is often linked to insulin resistance and hyperinsulinemia, which promote sodium retention and SNS activation results in increased BP (harder on CV system). impaired fasting glucose or insulin resistance represents pre-diabetic state in which body's cells become less responsive to insulin, leading to elevated blood glucose levels
76
how does adipose tissue dysfunction play a role in metabolic syndrome?
it secretes proinflammatory cytokines and adipokines that influence insulin sensitivity and vascular health. this chronic low-grade inflammation along with oxidative stress are key mechanisms driving development of metabolic syndrome "Factors such as pollution, cigarette smoke, poor diet, inflammation, and stress can contribute to oxidative stress"
77
management of metabolic syndrome
lifestyle mod (weight loss, exercise) pharm for controlling individual risks such as dyslipidemia, htn, hyperglycemia
78
what is hypothyroidism? associated with
when thyroid gland produces insufficient amounts of thyroid hormones. associated with bradycardia, increased PVR, elevated cholesterol levels (all add to risks of cardiovascular health)
79
symptoms of hypothyroidism
fatigue weight gain cold intolerance depression
80
what is myxedema coma?
severe hypothyroidism leading to decreased mental status, hypothermia, and other symptoms related to slowing of function in multiple organs.
81
what is hyperthyroidism? associated with
excessive production of thyroid hormones (T3 and T4) can result in tachycardia, atrial fibrillation, and increased CO
82
symptoms of hyperthyroidism
weight loss heat intolerance nervousness palpitations
83
what is thyroid storm?
life threatening exacerbation of hyperthyroidism that requires immediate medical attention
84
labs measured to test thyroid function
serum TSH T3 and T4
85
what labs indicate hypothyroidism?
elevated TSH Low T4
86
what labs indicate hyperthyroidism?
low TSH high T4
87
management of hyper and hypothyroidism
hypo: levothyroxine to normalize hormone levels hyper: antithyroid meds (methimazole or propylthiouracil), radioactive iodine therapy, surgery
88
two primary categories of coagulopathies
inherited and acquired
89
inherited coagulopathies
hemophilia von Willebrand disease
90
what is hemophilia?
deficiency in clotting factors VIII or IX, leading to prolonged bleeding
91
what is von Willebrand disease?
deficiency or dysfunction of von Willebrand factor (crucial for platelet adhesion and aggregation)
92
how do acquired coagulopathies result?
more common liver disease** vitamin K deficiency (bc used to synthesize certain clotting factors) DIC AC meds like warfarin or heparin
93
Dx of coagulopathies
lab tests: prothrombin time (PT) activated partial thromboplastin time (aPTT) platelet count specific assays for clotting factors
94
what is anemia?
condition characterized by deficiency in number or quality of red blood cells (RBCs) or hemoglobin, leading to decreased oxygen transport capacity in the blood heart must work harder to deliver adequate oxygen to tissues, could exacerbate cardiac conditions
95
classifications of anemia
iron-deficiency anemia vitamin B12 deficiency folate deficiency hemolytic anemia of chronic disease
96
describe iron deficiency anemia
most common due to insufficient iron intake or chronic blood loss results in microcytic hypochromic RBCs
97
vitamin B 12 and folate deficiencies lead to ____________ anemia. often result from
megaloblastic anemia (RBCs are larger than normal and fewer in number) poor dietary intake or malabsorption syndromes
98
what causes hemolytic anemia?
the premature destruction of RBCs can be due to autoimmune disorders, genetic conditions like sickle cell disease, or exposure to certain toxins
99
s/s of anemia
fatigue, pallor, DOE, tachycardia, palpitations in severe cases, can lead to angina or heart failure due to increase cardiac workload
100
dx of anemia
CBC reticulocyte count peripheral smear analysis additional tests may include: serum ferritin vitamin B12 levels folate levels tests for hemolysis markers
101
anemia management
underlying cause iron supplementation for iron deficiency anemia vitamin B12, folate supplements hemolytic anemia: corticosteroids, or immunosuppressants, blood transfusions
102
ischemic stroke can be thrombotic or embolic
thrombotic: clot forms at site of atherosclerotic plaque embolic: clot or debris travels from another part of the body to the brain *ischemic more common
103
hemorrhagic strokes result from bleeding either
within the brain (intracerebral) or in surrounding spaces (subarachnoid space)
104
causes of hemorrhagic stroke
high BP aneurysms arteriovenous malformations
105
what does FAST stand for?
Facial drooping Arm weakness Speech difficulties Time
106
what is the time window for tPA administration? (tissue plasminogen activtor)
4.5 hours from LKW
107
what is AKI?
sudden episode of kidney failure or kidney damage that occurs within a few hours or days, resulting in the accumulation of waste products in the blood and an imbalance of fluids and electrolytes.
108
pathophysiology of AKI
involves rapid decline in GFR, which leads tin an increase in serum creatinine and/or reduction in urine output.
109
three types of AKI
prerenal, intrinsic, postrenal
110
prerenal AKI
caused by decreased blood flow to the kidneys, often due to conditions such as heart failure or severe dehydration.
111
intrinsic AKI
direct damage to the kidneys, such as nephrotoxic drugs, acute tubular necrosis, or glomerulonephritis
112
postrenal AKI
from obstruction of urine flow, possibly due to kidney stones or tumors
113
s/s AKI
oliguria, edema, fatigue, confusion, nausea, elevated BP
114
dx of AKI
typically show elevated serum creatinine and blood urea nitrogen (BUN) levels UA may show proteinuira or hematuria
115
AKI management
cause maintaining fluid balance prevent further injury prerenal: restore adequate blood flow with fluids or meds intrinsic: dc nephrotoxic agents and manage hyperkalemia postrenal: relieve obstruction through catheterization or surgery
116
what is CKD?
progressive condition characterized by the gradual loss of kidney function over time. defined by a GFR of less than 60 mL/mn/1.73 m^2 for three months or more. can also be identified by markers of kidney damage, such as albuminuria, abnormalities in urine sediment, or structural abnormalities detected through imaging. systemic complications due to impaired function of the kidneys
117
CKD classifications
based on GFR levels. stage 1: normal or high GFR with evidence of kidney damage stage 5: kidney failure with GFR below 15mL/min, often needing dialysis or transplant
118
risk factors for CKD
DM HTN CV disease obesity family hx kidney disease (DM and HTN leading cause due to damage effects on renal blood vessels and tissues.
119
s/s CKD
subtle initially. fatigue, edema, htn, anemia, electrolyte imbalances (hyperkalemia and metabolic acidosis) uremic symptoms like nausea and cognitive disturbances
120
CKD management
underlying cause. Angiotensin-converting enzyme inhibitors (ACEIs) or angiotensin receptor blockers (ARBs) are commonly used to manage hypertension due to renal protective effects. dietary: protein restriction, monitoring intake of sodium, potassium, and phosphorus regularly monitor RFTs, electrolytes, BP
121
What is multisystem organ dysfunction syndrome (MODS)?
severe, life threatening condition characterized by progressive dysfunction of two or more organ systems, resulting from uncontrolled inflammatory response to injury or infection. can be triggered by various factors such as sepsis, trauma, severe pancreatitis.
122
general pathophys of MODS
systemic inflammatory response syndrome (SIRS) occurs, leading to widespread inflammation. results in endothelial damage and increased vascular permeability, causing fluid and protein leakage into tissues. consequently, there is impaired oxygen delivery and utilization at the cellular level, leading to tissue hypoxia and organ dysfunction.
123
how is heart impacted by MODS?
may suffer from myocardial depression due to inflammatory mediators such as cytokines and nitric oxide. this can lead to decreased CO and hypotension, which further exacerbates tissue hypoperfusion.
124
what is shock?
critical condition characterized by inadequate tissue perfusion, leading to insufficient oxygen and nutrient delivery to meet cellular demands.
125
what is hypovolemic shock?
occurs due to significant reduction in intravascular volume, commonly from hemorrhage or severe dehydration. the decreased circulating volume leads to reduced preload and cardiac output. compensatory mechanisms include vasoconstriction and tachycardia to maintain perfusion pressure.
126
what is cardiogenic shock?
resulting from hearts inability to pump effectively, this type often follows an acute MI. the impaired cardiac output results in inadequate tissue perfusion despite normal or increased intravascular volume. s/s include pulmonary congestion due to elevated left ventricular filling pressures.
127
what is distributive shock?
encompasses conditions like septic shock, anaphylactic shock, and neurogenic shock, where there is an abnormal distribution of blood flow due to vasodilation and increased vascular permeability. septic shock involves systemic infection leading to widespread inflammation and vasodilation. anaphylactic is an acute allergic reaction causing massive histamine release and vasodilation. neurogenic results from SCI, causing loss of sympathetic tone.
128
what is obstructive shock?
occurs when physical obstruction impedes cardiac filling or outflow, such as pulmonary embolism or cardiac tamponade. obstruction limits CO despite normal heart function.
129
what is non-cardiac chest pain (NCCP)?
term used to describe chest pain that resembles heart-related pain but is not caused by heart disease. can be equally distressing and may mimic angina, leading to concerns about potential cardiac events. often involves esophagus, musculoskeletal system, lungs, or psychological factors.
130
causes of NCCP: GERD
stomach acid irritates the esophagus. can result in burning sensation or discomfort in chest that is often mistaken for heart related pain
131
causes of NCCP: musculoskeletal issues
-like costochondritis or muscle strain -involve inflammation or injury to muscles and cartilage around ribs and sternum, causing sharp or aching pain that intensifies with movement or palpation
132
causes of NCCP: pulmonary conditions
like pleuritis or pulmonary embolism pleuritis: inflammation of pleura (lining surrounding lungs) leading to sharp pain during breathing or coughing PE: sudden and severe CP along with other symptoms like SOB
133
causes of NCCP: psychological factors
anxiety and panic disorders stress and anxiety can manifest physically, leading to chest tightness and discomfort that mimic cardiac symptoms.
134
chronic alcohol use impact on cardiac function
cardiomyopathy, arrythmias, hypertension
135
cocaine and amphetamines impact on cardiac function
increase heart rate and blood pressure, leading to increased risk of MI and stroke
136
nicotine impact on cardiac function
contributes to atherosclerosis and CAD by damaging endothelial cells and promoting platelet aggregation
137
alcohol withdrawal can lead to
autonomic instability with symptoms like tachycardia and hypertension, which may exacerbate existing cardiac conditions severe: DT. severe agitation and cardiovascular instabilty
138
cocaine withdrawal often presents with
fatigue, depression, increased appetite but can also cause cardiac complications due to persistent sympathetic stimulation during acute intoxication phases
139
nicotine withdrawal is associated with
increased anxiety and irritability, can temp elevate HR and BP.
140

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