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pale and sweat in heart disease
- 1. Explain and Correlate the Pathophysiology in Pale and Sweating
- 2. Coronary artery disease (CAD) • Impairment of blood flow through the coronary arteries • Most commonly by fatty atheroma (plague) • Risk factors : Smoking, Unhealthy(obese or overweight), High cholesterol, Sedentary lifestyle, Diabetes, Family history • Symptoms : vomiting, anxiety, angina, coughing, faint • Clinical presentations : silent ischemia, angina pectoris, acute coronary syndromes (unstable angina, myocardial infarction), and sudden cardiac death. • Diagnosis : by symptoms, ECG, stress testing, and coronary angiography • Treatment : drugs, procedures to reduce ischemia and restore or improve coronary blood flow.
- 3. Pathophysiology Coronary Artery Disease Asymptomatic Symptomatic Stable Angina Acute coronary syndrome Unstable Angina Non ST elevation myocardial infarction ST elevation myocardial infarction • Endothelium injury • Accumulation of lipoproteins • Monocyte adhesion to the endothelium • Platelet adhesion • Factor release • Smooth muscle cell proliferation & ECM production • Lipid accumulation
- 5. What is pallor? • It suggests the pale appearance of the skin. • Reduces blood flow & oxygen or decreases no. of RBC • It depends on the skin pigmentation & skin thickness. • Sites : face, oral mucosa, tongue, lips, conjunctiva, nail bed, palms & soles. • Causes : anemia, hypopituitarism, hypogonadism, left heart failure, shock, lack of sun exposure, common cold, blockage of artery • Symptom associated : fainting, fever, vomiting blood, rectal bleeding, abdominal pain Anemia Acute Rapid heart rate Shortness of breath Chest pain Low blood pressure chronic Poor nutrition Heavy menstrual bleeding Diagnosis Tests • Complete Blood Count (CBC) • Stool culture • Thyroid function test • Kidney function test • Vitamin deficit test • X-ray • Ultrasound • CT scan Treatments • Iron, vitamin B12 or folate • Medication
- 6. • The release of a salt-based fluid from sweat glands. • Function : regulate body temperature. • Causes : temperature, medication, food, or emotional state. • Effects : heat exhaustion, heat stroke, hyperthermia & death • Sites : armpits, face, palms & soles • Mechanism : - • Hypothalamus (thermoregulatory) controls blood flow & sweat output. • It is triggered by exercise, temperature change, hormone & stress. • Message sends to the spinal cord via neurotransmitters (acetylcholine, catecholamine). • Neurotransmitters travel down to ganglion to nerves innervating the skin’s surface. • Excessive sweating – Diaphoresis / Hyperhidrosis What is sweating (perspiration)? Sweat glands eccrine Independent of hair follicle apocrine Attached to hair follicles apoeccrine Precursor glands Increase in skin temperature Increase in core temperature Stimulates preoptic hypothalamus Sweating, vasodilation & rapid breathing
- 7. Pathophysiology of Diaphoresis • Same in number & size of glands • Hyper function of sweat gland, hyperactive to thermal stimulus • Extreme, uncontrollable sweating • Excessive sympathetic activity • palmoplantar hyperhidrosis - less reflex bradycardia in response to Valsalva maneuver or facial immersion than healthy controls, but a higher degree of vasoconstriction in response to finger immersion in cold water.This shows the increased sympathetic activity through the T2-T3 ganglia. • Hyperexcitable somatosympathetic polysynaptic pathway • Normal eccrine glands produce sweat in response to stimuli, such as elevated temperature, physical activity, and stress or anxiety • These responses are controlled by the central nervous system through activation of the hypothalamus, resulting in release of acetylcholine at the neuroglandular junction
- 8. 1. Influenza • High fever in adults & children Antibiotics 2. Chronic kidney failure 3. Anemia 4. Cancers : colon cancer, renal cell cancer, and multiple myeloma 5. Heart issues: heart disease, heart infection, heart attack, or heart failure • chest pain, shortness of breath, nausea or pain in the back, neck, jaw or arm 6. Artery blockage • Hypoglycemia 7. Diabetes 8. Stress 9. Medication • Painkillers, cardiac and gastrointestinal medicines 10. Animals/insects bite • risk of anaphylaxis (hypersensitivity) Complications of Pallor and Sweating When Does Excessive Sweat Sometimes Accompany Pallor?
Editor's Notes
- Also known as Atherosclerotic cardiovascular disease (ASCVD) Coronary atherosclerosis Coronary heart disease Ischemia heart disease Coronary atherosclerosis – abnormal accumulation of lipid or plague in the lumen of coronary artery
- 3 layers - Tunica intima, media, adventitia (intima-atherosclerosis form) Blood flows through the artery contains the red blood cells and lipids (LDL). LDL adhere to the artery wall and grows overtime Usually asymptomatic until the plaque becomes larger Artery becomes narrow and blood flow to the heart becomes restricted. Stable angina - artery is blocked enough to slightly impede blood flow Chest pain - during activity Pressure - blood flow - oxygen Atherosclerosis Hardening of artery Narrowing due to plague (LDL) X arteriosclerosis (hardening of artery only) Plague suddenly rupture - coronary thrombosis – acute coronary syndrome Non ST-segment elevation myocardial infarction Unstable angina -Myocardial ischemia at rest -Electrocardiogram- ST segment depression Thrombus completely occludes the vessel, myocardial injured & ST segment elevation myocardial infarction develops. Pathophysiology Atherosclerosis is an inflammatory process which predisposes individuals to ACS. It is a complex cellular process involving lipids, macrophages and smooth muscle. Step 1 - endothelial dysfunction The first step is endothelial injury. This causes a local inflammatory response. If the injury recurs or healing is incomplete, inflammation may continue leading to the accumulation of low-density lipoproteins (LDL). These become oxidised by local waste products creating reactive oxygen species (ROS). Step 2 - plaque formation In response to these irritants, endothelial cells attract monocytes (macrophages). These engulf (phagocytose) the LDLs swelling to become foam cells and ‘fatty streaks’. Step 3 - plaque rupture Continued inflammation triggers smooth muscle cell migration. This forms a fibrous cap, which together with the fatty streaks, develops into an atheroma. The top of the atheroma forms a hard plaque. This may rupture through its endothelial lining exposing a collagen-rich cap. Platelets aggregate on this exposed collagen forming a thrombus that may occlude or severely narrow the vessel. Alternatively, the thrombus may break lose, embellishing to infarct a distant vessel.
- 1.6 – 4 million sweat glands on the body
- 1. Influenza 2. Kidney Infections 3. Anemia 4. Heat Exhaustion 5. Alcohol or Drug Withdrawal 6. Cancer 7. Chronic Infections 8. Venomous or Severe Bites 9. Arterial Blockage 10. Diabetes 11. Heart Conditions 12. Hypoglycemia 13. Thyroid Problems 14. Anxiety 15. Medications