Diseases Flashcards
Costochondritis
- Inflammation of the cartilage connecting a rib to the sternum
- S/S:
- Sharp pain at the connection
- Can mimic heart attack
- reproducible tenderness when pressing on rib joints
- pain can be aggravated by exercise, minor trauma, or upper respiratory infection
- usually sharp pain located on front of chest wall, it may radiate to the back or abdomen.
- Pain is worse with movement, exertion and deep breathing
- Causes:
- Usually unknown
- Trauma
- Physical strain
- May affect females more than males
- Tx:
- Anti-inflammatory drugs (i.e. Ibuprofen)
Angina Pectoris
- Chest pain caused by reversible myocardial ischemia
- S/S:
- Sudden severe chest pain lasts 3-5 minutes
- Pressure/squeezing
- Fatigue, Nausea, Shortness of Breath
- Causes:
- Cardiovascular disease
- Anemias
- Tx:
- Rest
- Nitrates – dilate arteries and veins
Myocardial ischemia
Develops if flow or O2 content of coronary blood is insufficient to meet the metabolic demand of myocardial cells
- most common cause of decreased coronary blood flow & resultant myocardial ischemia is formation of atherosclerotic plaques in coronary circulation
- as plaque increases in size, it may partially block vessel lumina limiting coronary flow & causing ischemia, especially during exercise
- some plaques unstable=prone to ulceration/rupture. If this occurs underlying tissues of vessel wall are exposed resulting in platelet adhesion & thrombus formation
- thrombus formation can suddenly stop blood supply resulting in acute myocardial ischemia & if vessel obstruction can’t be reversed rapidly it will progress to infarction
- Myocardial ischemia can also result from other causes of decreased blood & O2 delivery to myocardium:
1) coronary spasm
2) hypotension
3) dysrhythmias
4) decreased O2 carrying capacity of blood (anemia, hypoxemia) - Myocardial cells become ischemic w/in 10 seconds of coronary occlusion, thus hampering pump function & depriving myocardium of a glucose source for aerobic metabolism. Anaerobic takes over & lactic acid accumulates
- cardiac cells remain viable for approx. 20 min under ischemic conditions
- if blood flow is restored, aerobic metabolism resumes, contractility is restored & cellular repair begins. If not restored MI occurs
Define atherosclerosis and what disease would you find it in?
Atherosclerotsis are the formation of plaques in the coronary circulation that my occlude the vessel lumina and cause a blockage and lead to myocardial ischemia (Angina pectoris)
What is the DDx between angina pectoris and a heart attack?
For both, there are elevated levels of CRP, but angina pectoris lasts for 3-5 minutes
SUPER HELPFUL HINT: Hyper/Hypo Kalemia is potassium levels
Hyper/Hypo NAtremia is for sodium levels
…
If an EKG shows prolonged waves, which of the following would it represent? A. Hyponatremia B. Hyperkalemia C. STEMI D. Hypokalemia B. Hyperkalemia
B. Hyperkalemia
A patient comes in complaining of coughing up blood. An endoscopy is done and it is found that stratified columnar is growing in his esophagus. What would this represent? A. Metaplasia B. Hypertrophy C. Hyperplasia D. Dysplasia A. Metaplasia
A. Metaplasia
Helpful to remember: Hyperplasia is related to pregnancy/menstrual cycle
A man comes in to the ER with a headache and low levels of ADH. He is complaining of constant urination- Would we expect his serum osmolarity be high or low?
High- the assumption is made off of the assumption that he has DI
A 65-year-old man comes in with acute chest pain, and pain radiating down his left arm. An EKG was done and it came back signifying an ST elevation. How many layers of the heart were affected? Why? In the previous case, (STEMI) which cardiac enzyme would be elevated?
Three layers of the heart were effected, because the ST elevation signifies a STEMI.
Troponin I and T
(this is an intentionally non-specific question) A person comes into the ER with chest pain, and when tested they come back with a normal EKG. Their chest is sensitive to palpation, and their pain lasted for six hours after they were discharged. What do you think the diagnosis was?
Costochondritis
a 75-year-old male is suffering from difficulty breathing, blue skin, and slight chest pain. They notice a clot in the R. Bronchiole. What is this clotting issue called?
Ischemia!
Types of angina pectoris
Stable angina: effort, typical - atherosclerosis > exercise, emotion, heavy meal > pain
Unstable angina: accelerated > severe type. decrease change in pattern and an increase frequency and/or duration of pain
Variant angina: prinzmetal > a-receptor mediated V.C. (with or w/out atherosclerosis) > pain even at rest
Stable angina pectoris
Cause: Gradual luminal narrowing & hardening of arterial walls, so that affected vessels cannot dilate in response to increased myocardial demand associated w/physical exertion or emotional stress
-w/rest blood flow is restored & no necrosis occurs
S/S: typically experienced as transient substernal chest discomfort, ranging from a sensation of heaviness or pressure to moderately sever pain. The sensation is often described by clenching a fist over the left sternal border.
-discomfort may be mistaken for indigestion
-pain is caused by buildup of lactic acid or abnormal stretching of the ischemic myocardium that irritates myocardial nerve fibers. These afferent fibers enter the spinal cord from levels C3 to T4, accounting for a variety of locations & radiation patterns of anginal pain. discomfort may radiate to neck, lower jaw, left arm, and left shoulder, occasionally to the back or down the right arm.
-Pain associations: Pallor (pale skin), diaphoresis, and dyspenia
-Pain in women: may not have typical pain. Atypical chest pain, palipitations, sense of unease, severe fatigue
-Pain seen in autonomic nervous system dysfunction (older adults, diabetes) angina may be mild, atypical, or silent
Tx: Rest & nitrates; lack of relief may indicate MI
Variant angina (prinzmetal)
Chest pain attributable to transient ischemia of the myocardium that occurs unpredictably & often at rest
- Pain caused by vasospasm of one or more major coronary arteries w/or w/out atherosclerosis
- Pain often occurs at night during rapid eye movement sleep & may have a cyclic pattern of occurrence
- Angina may result from decreased vagal activity, hyperactivity of the sympathetic nervous system, or decreased nitric oxide activity
- Other causes: altered Ca++ channel function in arterial smooth muscle or impaired production or release of inflammatory mediators (serotonin, histamine, endothelin, thromboxane)
- Serum markers of inflammation (CRP) & interleukin-6 are elevated
- Usually benign condition, but can occasionally cause serious dysrhythmias
Silent ischemia & mental stress-induced ischemia
Myocardial ischemia may not cause detectable symptoms such as angina. Ischemia can be totally asymptomatic and referred to as silent ischemia
- May be fatiqued, dyspnea, or a feeling of unease
- silent ischemia & atypical symptoms more common in women
- some only have silent ischemia & episodes of silent ischemia common in those who also experience angina
O2 supply to heart vs. demand
Decrease coronary blood flow:
Mechanisms that decrease blood flow include; vasospams (artery becomes smaller), fixed stenosis (narrowing of arteries lumen), Thrombosis (blood clots reduce blood flow)
ALL THESE LEAD TO ANGINA (CHEST PAIN)
Increase O2 Consumption
Mechanisms that increase O2 consumption include: Heart rate increases, heart contractions stronger, BP increases
ALL THESE LEAD TO ANGINA (CHEST PAIN)
Nitroglycerin mechanisms
1) Dilation of coronary vessels __________ oxygen supply to the myocardium
2) At low doses, nitroglycerin will dilate veins more than arteries, thereby _________ preload
Dilating the veins ___________ cardiac preload and lowers the oxygen requirement of the heart
3) At higher doses, it also dilates arteries, thereby ___________ afterload
The lowering of pressure in the arteries ___________ the pressure against which the heart must pump, thereby decreasing afterload and again, lowers the oxygen requirement of the heart
Overall effects:
Nitroglycerin was first used by William Murrell to treat anginal attacks in 1878, with the discovery published that same year
1) Dilation of coronary vessels Increases oxygen supply to the myocardium
2) At low doses, nitroglycerin will dilate veins more than arteries, thereby increasing preload
Dilating the veins increases cardiac preload and lowers the oxygen requirement of the heart
3) At higher doses, it also dilates arteries, thereby decreasing afterload
-The lowering of pressure in the arteries decreases the pressure against which the heart must pump, thereby decreasing afterload and again, lowers the oxygen requirement of the heart
Overall effects:
Decreases chest pain,
Decrease of blood pressure
Increases heart rate
Orthostatic hypotension
Tolerance - It has been shown that continuous exposure to nitrates can cause the body to stop responding normally to this medicine. Experts recommend that the patches be removed at night, allowing the body a few hours to restore its responsiveness to nitrates. Shorter-acting preparations can be used several times a day with less risk of the body’s getting used to this drug.
Tests for Angina pectoris
Tests - EKG – may be normal - Stress Tests (treadmill) - Coronary Angiography and Cardiac Catheterization * Dye w/X-rays to show coronary lumen CBC -Increase cholesterol -Increased C-reactive protein (CRP)? * Indicates inflammation somewhere in the body * Increased risk for heart attack - Anemia
What is C-Reactive protein?
C-Reactive protein is a test that can measure the level of C-Reactive protein (CRP) in your blood, increases when there is inflammation in your body. A simple blood test measures CRP. A high level of CRP in the blood is a sign that there may be an inflammatory process occurring in the body. High CRP levels may put patients at increased risk for coronary artery disease, which can cause a heart attack. CRP is a substance produced by the liver in response to inflammation.
What condition causes chest pain, nausea and shortness of breath but blood tests show no troponin or myoglobin in the blood?
What condition causes chest pain, nausea and shortness of breath but blood tests show no troponin or myoglobin in the blood? Angina Pectoralis
what condition does myocyte necrosis occur?
Myocardial infarction
What condition causes fatigue, nausea, shortness of breath, sudden sever chest pain and can be caused by anemias or cardiovascular diseases?
Angina Pectoris
Myocardial infarction
-AKA “Heart Attack”
MI is Blockage of coronary artery and anything distal to that blockage dies.
You have to have significant blockage before you even feel anything.
-Progressive ischemia with damage to myocardium (myocyte necrosis)
-2 types
1) Subendocardial MI
Thrombus dislodges and only myocardium directly beneath endocardium involved
2) Transmural MI
Thrombus remains and myocardium involved transcends to epicardium
Signs and symptoms of MI
S/S: Dyspnea Sudden severe chest pain with radiation Nausea/Vomiting Anxiety/dizzy/cough Diaphoresis – profuse sweating Heart Attack Video Clip Causes: Cardiovascular disease
When a person suffers from angina pectoris, what might their blood tests show?
Potential anemia or cholesterol levels and an increase in c-reactive proteins.
If a person has an anion gap, what other condition will they always be diagnosed with?
Metabolic acidosis
What are some signs and symptoms of a heart attack in women?
Jaw pain, back pain, nausea or vomiting
What condition causes serum osmolality to decrease and urine osmolality to increase?
SIADH
What is the treatment for MI
- Angioplasty
- Real angioplasty
- Thrombolytic therapy w/in 3 hours (clot breakdown)
- Cardioprotection after MI: Beta blockers (blocks sympathetic innervation), ACE inhibitors
Tests given for MI
Tests:
- BP – Initially decreases
- SNS reflexively activates:Temporarily increases HR and BP
- Abnormal extra heart sounds – LV dysfunction
- Pulmonary congestion: Dull percussion, Inspiratory crackles at lung bases
- Blood test values increased
1) Troponin I & T – lasts 1 week (most specific)
2) LDH – Lactic dehydrogenase
3) CK-MB – Creatine kinase-myocardial bound - Lasts 48 hours
- Less specific
- May be elevated in COPD, 3rd degree burns
3) Myoglobin – lasts 24 hours - Not specific for cardiac muscle
How to differentiate between costochondritis & MI
Elevated Troponin I levels would be sufficient to differentiate costochondritis from an MI
In MI Their BP will drop because if a portion of your heart can’t contract with as much force. Later on the somatic nervous system (sympathetic) kicks in and their BP temporarily increases.
When you have any muscle contract the calcium binds to troponin which allows it to contract. Troponin I and T in the heart.
If the heart muscle dies it spues its contents into the blood stream which means that you will see an increase of?
troponin, ldh, ck-mb, and myoglobin (not specific) Troponin I (gold standard, very specific)
How long does it take for troponin I to peak?
Cereal troponin I draw blood every 4-6 hours to see if it ?
- How long does it take for troponin I to peak? About 24 hours
- raises. It is very specific GOLDEN STANDARD
- Kidneys clear out Troponin i
CABG
The Coronary Artery Bypass Graft (CABG) involves bypassing major blocks in the blood vessels of the heart to improve the blood to the cardiac muscle (myocardium). The conduits used for bypass grafting can be veins taken from the legs or arterial conduits which include the mammary arteries from the chest wall, the radial artery from the forearm and an artery from near the stomach.
What condition can be caused by alcoholism, gallstones or trauma?
Pancreatitis
What type of MI is a non-STEMI?
A heart attack that involves just the innermost layer of the heart. I.E. Subendocardial MI
What is hyponatremia?
When sodium levels are too low In the blood
What are some causes of hyponatremia?
Vomiting, diarrhea, increased dietary sodium intake, excessive sweating
What is hypernatremia?
When sodium levels are too high in the blood
What are some causes of hypernatremia?
Diabetes insipidus, dehydration, over secretion of aldosterone.
What is hypokalemia?
Hypokalemia is where potassium levels in the blood are too low.
What are some causes of hypokalemia?
Some causes include: Decreased potassium intake
Alkalosis
Increased potassium loss throughout the body
What are some signs and symptoms of hypokalemia?
Muscle weakness
Cramps
Shallow T-wave (Causes tachycardia)
Mnemonic for hyperkalemia: MURDER (signs) MACHINE (causes)
Signs & Symptoms MURDER M - Muscle weakness U - Urine, oliguria, anuria R - Respiratory distress D - Decreased cardiac contractility E - ECG changes R - Reflexes, hyperreflexia, or areflexia (flaccid)
Causes MACHINE
M - Medications - ACE inhibitors, NSAIDS
A - Acidosis - Metabolic and respiratory
C - Cellular destruction - Burns, traumatic injury
H - Hypoaldosteronism/ hemolysis
I - Intake - Excessive
N - Nephrons, renal failure
E - Excretion - Impaired
What is the ECG for hyperkalemia
- When serum K+ mEq/L is at 7-High T wave
- When serum K+is at 8 mEq/L- Prolonged PR interval, depressed ST segment, high T wave
- When serum K+ is at 9 mEq/L- Auricle standstill, intraventricular block
- When serum K+ is at 10 mEq/L- Ventricular fibrillation
What is the ECG for hypokalemia
- When serum K+ is at 3.5 mEq/L- Low T wave
- When serum K+ is at is at 3 mEq/L- Low T wave, high U wave
- When serum K+ is at 2.5 mEq/L- Low T wave, high U wave, low ST segment
Hypokalemia:
1) Magnesium and Potassium have a?
2) Low magnesium stimulates?
1) Direct relationship
2) The release of renin which causes aldosterone to increase & causes K+ to be excreted by kidneys
Hyperkalemia:
Too much K+ in the ECF stimulates the release of?
Increase catecholamine levels and causes aldosterone levels to increase as a result K+ travels into the kidneys to be excreted by urine.
Diagnosis of hyperkalemia
- Serum K+ levels
- ECG monitoring
- ABG may reveal acidosis- correct this, K+ will correct
Medical management for hyperkalemia
- ECG
- Serum K+ redraw to confirm
- Restrict dietary K+ and salt substitutes
- Kayexalate- PO or enema; binds with K+ in GI tract for elimination
Appendicitis definition
Inflammation of the vermiform appendix.
-Most common surgical emergency of the abd and affects 7-12% of the population. Generally occurs between 20 & 30 years of age, although it may develop at any age
Pathophysiology of appendicitis
- Exact mechanism is controversial
- Obstruction of lumen w/stool, tumors, or foreign bodies w/consequent bacterial infection
- Obstructed lumen doesn’t allow drainage of appendix, as mucusal secretion continues, intraluminal pressure increases. Increased pressure decreases mucosal blood flow & appendix becomes hypoxic
- Mucosa ulcerates, promoting bacterial or other microbial invasion w/further inflammation and edema
- inflammation may involve distal or entire appendix
- Gangrene develops from thrombosis of the luminal blood vessels, followed by perforation
Clinical manifestations of appendicitis
- Gastric or periumbilical pain
- Pain may be vague at first, increasing in intensity over 3-4 hours
- Pain may subside & then recur in RLQ indicating extension of the inflammation to surrounding tissues
- N/V
- Diarrhea
- Constipation
- most serious complications: perforation, peritonitis, and abscess formation
Evaluation and treatment for appendicitis
- Can usually locate painful site w/one finger
- rebound tenderness usually referred to RLC
- Increased WBC count ranges from 10,000 to 16,000 w/increased neutrophils
- UT (ultrasonography), CT scans can assist in differentiating appendicitis from perforated ulcer or cholecystitis
- Laparoscopic appendectomy is treatment for simple or perforated appendicitis
- Surgery provides quick recovery for simple appendicitis
Appendicitis (all main points)
-Inflammation of appendix
-Causes
* Build up of mucus/stool > fecalith > inf. > immune response
-S/S
* Because the innervation of the appendix enters the spinal cord at the same level as the umbilicus (belly button), the pain begins stomach-high. As the appendix becomes more swollen and inflamed, it begins to irritate the adjoining abdominal wall. This leads to the localization of the pain to the right lower quadrant. This classic migration of pain may not be seen in children under three years.
* Perforation > Peritonitis/Sepsis
* Intestinal Ileus - blockage
-Testing
* CBC
↑WBC’s due to infection
* CT
* US – can only see 50% of appendicitis
-but can check ovary in women at the same time
* X-ray – may see fecalith
* CRP
-Tx
* Surgery
Causes:
1) Obstruction
2) IBD (Inflammatory Bowel Disease)
3) Infection
4) Fecal stasis
Appendicitis
Signs and symptoms of appendicitis
1) Acute (first 48 hours and not ruptured)
2) RLQ abdominal pain
3) Rebound tenderness
4) Fetal position (unwillingness to stretch out legs)
5) Pain w/movement
6) Fever
7) N/V
8) Loss of appetite
9) Elevated WBC
Ruptured appendix
- Abd pain for 2-3 days then sudden relief (at time of rupture)
- Within a few hours of rupture:
- sever diffuse pain
- N/V/D
- Fever
- Sepsis
- Fetal position
- Guarding
Peritonitis (main points)
-Infl. of serosa and organs > covering
- Causes
* Inf > perforation of bowel, appendix, ulcer (gastric acid), pelvis (inf. fallopian tube), malignancy, trauma, pancreatitis
- S/S
Abd. Pain, inf. sxs fever, tachycardia
Dehydration shock
Rigid abd.
Infl fibrosis adhesions
- Testing
CBC, UA, Amylase/Lipase, BC
CT
A 22 year old female recently endured a successful abdominal surgical procedure. After safely returning to her home, she began to experience a mild fever, feeling bloated, and an aching pain in her abdominal region. She immediately returned to the hospital where manual palpation suggest a stiff abdominal painful to the touch and possible inflammation. She had tachycardia, tachypnea, and her blood pressure was 80/60 right before she apparently went into shock. What was the probable cause of her symptoms?
a. Appendicitis
b. Peritonitis: lignin of the abdomen region. Rigid stomach → peritonitis
c. Nephrolithiasis
d. pancreatitis
b. Peritonitis: lignin of the abdomen region. Rigid stomach → peritonitis
Signs and symptoms of peritonitis
- Can mimic hypovolemia
- Abd pain
- Fever
- Tachycardia/tachypenia
- Dehydration which can lead to shock
- Rigid abdomen and distention
- perfusion issues
- Rebound tenderness
- anorexia
- N/V
- Decreased bowel sounds
- Low BP
What are the causes of peritonitis
- Abd surgery
- Inflammation that could lead to perforation of bowel
- perforation from appendix, ulcer
- pelvis (inf. of fallopian tube)
- malignancy (tumor)
- trauma
- pancreatitis
Tests given for peritonitis
- CBC (may show high WBC)
- CT scans and X-rays
Nephrolithiasis (main points)
- Kidney Stones
- Calcium Oxalate, Struvite (Mg)
- Uric Acid
- Causes
- M 12%>F 5% (30-50% get a second one) and age
- Dehydration
- Abnormal Calcium metabolism
- Hypercalciuria –hyperabsorption of dietary calcium
- Prolonged immobiliazation – bone demineralization
- S/S
- Flank (Renal colic) or Abdominal pain
- N/V, Dysuria, Hematuria,
- Testing
- UA, CT now, used to be IVP (Intravenous pyelogram)
an X-ray of the abdomen along with the administration of contrast dye into the bloodstream - Renal Function > BUN, Creatinine (by-product muscle metabolism), Uremia
- Calcium: Parathyroid Hormone
- UA, CT now, used to be IVP (Intravenous pyelogram)
Treatment for peritonitis
- Surgery (Decrease abd distention)
- Administer antibiotics (for infection)
- To decrease amount of fluid going into peritoneal cavity, give patient NG tube (nasogastric tube) to suck out and decompress the bowels
- Give them added IV fluids (isotonic fluids) to make sure patient is not becoming severely hypovolemic
When a T wave is below threshold what is this signature of?
T wave is below threshold is the signature for subendocardial MI.
Edema
Excessive Accumulation Of Fluid In The IS (Interstitial Spaces)
- Localized - due to trauma or around an organ
i. e. pulmonary edema - Generalized - uniform distribution of fluid
i. e. due to CHF
Hormones regulating fluid balance
1) ADH -Anti-Diuretic Hormone - ↓water loss (less ADH=urinate more)
2) Aldosterone – reabsorb Na+, excrete K+ (high aldosterone is a Na+ saver so water follows which makes BP go up)
3) ANP - Atrial Natriuretic Peptide hormone
4) BNP - Brain (B-type) Natriuretic Peptide hormone
First discovered in the brain, but released by heart ventricles
- ANP & BNP stimulate
Renal elimination of Na+
ANP made in atrium of heart. Sodium lose in urine water follows drop blood pressure
BNP made in ventricle of heart it decreases sodium and water follows
ANP & BNP Drops?
ANP made in atrium of heart. Sodium lose in urine water follows drop blood pressure
BNP made in ventricle of heart it decreases sodium and water follows
ANP & BNP Drops blood pressure
Blood pressure changes in response to hormonal flucutations ↑ Aldosterone = _?_ BP Increase BP ↑ ADH = _?_ BP Increase BP ↑ ANP = _?_ BP Decrease BP ↑ BNP = _?_ BP Decrease BP
Increase Aldosterone= INCREASE
Increase ADH= INCREASE
Increase ANP= DECREASE
Increase BNP= DECREASE
Capillaries: Arteriole end venule end
- Arteriole end
- High hydrostatic pressure in the blood
- Relatively low osmotic pressure in the blood
- Hydrostatic pressure wins at this end of capillary: Fluid moves out
Net FILTRATION - Venule end
- Low hydrostatic pressure in the blood
- Relatively high osmotic pressure wins at the end of capillary. Fluid moves into the blood
- Net re-absorption
