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
Albumin (which is made by the liver) creates pressure in the capillaries. If a cell is filled w/Albumin you have a hypotonic cell. The concentration of the fluid outside the cell is less than the concentration inside the cell so water moves in towards concentration. So what happens if we have albumin in the capillaries?
So if we have a problem w/the liver it’s going to create a problem with albumin and that might create a problem with edema
It’s going to want to draw water from the outside towards the albumin. This is called OSMOTIC PRESSURE OF THE CAPILLARY.
- Osmotic pressure stays the same at both ends hydrostatic pressure does not
Causes of edema
1) Increased hydrostatic pressure:
a) any kind of kidney failure that leads to water retention
b) hyperaldosteronism-anything that causes hypernatremism (too much Na+) can cause retention of Na+ which is going to cause increase reabsorption of water and too much fluid in the arterioles that will increase pressure there
c) high venous pressures:
- if anything is blocking venules the pressure will build back up to capillaries and force fluid out causing edema. Heart failure can do this or venous obstruction or failure of venous valves
- failure of venous pump: paralysis of muscles, immobilize a body part
d) decreased arterioler resistance
2) Decreased plasma proteins
a) decrease or loss of protein in urine
b) can lose protein via denuded skin (burn or wound)
c) failure to make proteins (due to liver failure, serious protein, or caloric malnutrition)
3) Increased capillary permeability
a) immune reaction that release histamine which stimulates inflammation by opening up capillary permeability
b) any kind of toxin
c) Bacterial infections
d) vitamin deficiency
e) burns
f) prolonged ischemia
4) Blockage of lymphatic return
a) cancer
b) infection
c) surgery
d) congenital absence or abnormality
Causes of edema
- Increase Capillary filtration (increase capillary BP or permeability)
- Poor venous return
- Congestive heart failure - pulmonary edema
- Insufficient muscular activity
- Kidney failure (water retention, hypertension)
- Histamine makes capillaries more permeable
- decrease Capillary reabsorption
- Hypoproteinemia (oncotic pressure blood albumin) cirrhosis, famine, burns, kidney disease
- Obstructed lymphatic drainage
Left Heart Failure
Inability of left side to pump into systemic circulation
1) R ventricular output exceeds left ventricular output
2) Pressure backs up
3) Fluid accumulates in pulmonary tissue
Right heart failure
Inability of right side to adequately pump venous blood into pulmonary circulation.
1) Left ventricular output exceeds right ventricular output
2) Pressure backs up
3) Fluid accumulates in systemic tissue
SIADH Syndrome Of Inappropriate ADH Secretion
- Excessive secretion of ADH
- Causes
Idiopathic
Brain injury, infection, trauma, stroke, hemorrhage
ADH secreting tumor (bronchogenic cancer *most common)
Signs and Symptoms
Hyponatremia (does this make sense?)
Dilutional hyponatremia from water intoxication
Testing
↓Serum osmolarity vs.↑Urine osmolarity
Too much TBW should lead to more urine, right?
The low serum osmolarity suppresses Renin
and Aldosterone so Na+ is not reabsorbed. More concentrated urine results
CT/MRI – tumor?
Cholelithiasis (Gallstones)
- Definition: Obstruction of gallbladder caused by gallstones. It is gallstone formation.
- Normal pt’s: Prevalent disorder in developed countries where incidence is 10-15% in white adults & 60-70% in Native Americans.
- Two types: cholesterol (most common), pigmented
- Risk factors: Obesity, middle age, female, use of oral contraceptives, rapid weight loss, Native American ancestry, genetic predisposition, & gallbladder, pancreatic, or ileal disease
- S/S: Often asymptomatic, abdominal pain & juandice are cardinal manifestations.
- Vague symptoms: heartburn, flatulence, epigastric discomfort, & food intolerances (particularly to fats and cabbage)
- pain (biliary colic) occurs 30min-several hours after eating a fatty meal. Caused by lodging of one or more gallstones in cystic or common duct
- Usually RUQ, can be intermitten or steady, radiating to mid-upper area back
- Juandice=stone in common bile duct
- Test: Physical exam, ultrasound, or CT, oral cholecystogram
Signs/Symptoms of Cholelithiasis (gallstones)
Often asymptomatic, abdominal pain & juandice are cardinal manifestations.
- Vague symptoms: heartburn, flatulence, epigastric discomfort, & food intolerances (particularly to fats and cabbage)
- pain (biliary colic) occurs 30min-several hours after eating a fatty meal. Caused by lodging of one or more gallstones in cystic or common duct
- Usually RUQ, can be intermitten or steady, radiating to mid-upper area back
- Juandice=stone in common bile duct
Cholecystitis (main points)
- Inflammation of Gallbladder
- Causes
- Female, Overweight/Obese, Reproductive Age, 40’s
- S/S
- RUQ pain > R lower shoulder blade (referred)
- N,V, Fever and chills
- Testing
- Positive Murphy’s sign
- US, CT
- DDX:
- Pancreatitis – ↑Amylase, Lipase
- Tx:
- Surgery
Positive Murphy’s sign
Cholecystitis
How to test for peritonitis
CBC, UA, Amylase/Lipase, BC (blood culture), CT
Risk factors for peritonitis
- Abd surgery
- Ectopic pregnancy
- Perforation: Trauma, ulcer, appendix, diverticulum
Ovarian cysts
- Fluid filled sacs
- Most are benign
- Ovarian cancer accounts for 4% of all cancers for women
- Causes
1) Hormone imbalance
2) Prior ovarian cysts
3) BC pills reduce risk of ovarian cysts due to preventing ovaries from producing eggs during ovulation - S/S
1) Usually do not have pain symptoms
2) Lower abdominal or pelvic pain
3) Lower abd or pelvic ‘fullness’ or pressure sensation - Pain may indicate rupture
- Testing
1) US (ultra sound) - Tx
- Usually resolve on their own
- Anti-inflammatory – reduce pain
- Pain meds
- Surgery for removal if it lasts longer than a few months
S/S of ovarian cyts
S/S
1) Usually do not have pain symptoms
2) Lower abdominal or pelvic pain
3) Lower abd or pelvic ‘fullness’ or pressure sensation
- Pain may indicate rupture
Testicular torsion
- Twisting of spermatic cord
- Causes
- Trauma, Sports, Exercise
- most common among neonates and adolescents
- 90 to 180 degrees is enough to ↓ blood flow
- S/S
- Unilateral acute onset pain
- Swelling/pain=acute scrotum
- N/V
- Testing
- Urinalysis (for infection)
- Color Doppler ultrasonography
- Tx
- Within 6 hours to preserve normal testicular function
- Manually de-torse
- Surgery – suture for future prevention must be performed w/in 6 hrs after onset of symptoms
Gout
- Uric acid crystal deposition
(Ben Franklin suffered from it)
-Causes - Increase uric acid levels, usually due to underexcretion of uric acid by the kidney
- Inherited abnormality of handling uric acid
- Obesity
-S/S - Painful joint inflammation - big toe mostly
- Typically attack one joint at a time
- Tophi (Untreated gout may cause deposits of urate crystals to form under the skin in nodules called tophi. Tophi can develop in several areas such as your fingers, hands, feet, elbows or Achilles tendons along the backs of your ankles. Tophi usually aren’t painful, but they can become swollen and tender during gout attacks
- Kidney stones – more frequent
-Testing - RF (rule out RA),
- Arthrocentisis - Joint aspiration -Uric acid
- X-Ray
What condition would you see hyperuricemia (excess serum uric acid levels)?
Gout
What will cause hyperuricemia?
Excessive uric acid production or underexcretion of uric acid by the kidneys
Underexcretion of uric acid is responsible for about 90% of the cases of elevated uric acid level. When uric acid reaches a certain concentration in fluids, it crystallizes, forming insoluble precipitates that are deposited in connective tissues throughout the body. Crystallization in synovial fluid causes acute, painful inflammation of the joint, a condition known as?
-With time, crystal deposition in subcutaneous tissues causes the formation of small, white nodules, or?
Gouty arthritis.
Tophi, that are visible through the skin
In classic gouty arthritis, monosodium urate crystals form and are deposited in joints and their surrounding tissues, initiating a?
Inflammatory response
Gout is rare in children and premenopausal women and is uncommon in males younger than 30.
What are risk factors for gout?
1) Male gender
2) increasing age
3) high intake of alcohol, red meat, and fructose
- peak age of onset in males is between 40 & 50
- risk of developing gouty arthritis is same for males/females
- females tend to have onset at later age & have greater use of diuretics
Single most important determinant of the risk of developing gout?
Plasma urate concentration
ADH (also called vasopressin): Anti-diuretic hormone Functions
1) Regulates body water (so it controls the kidneys & it controls how much water the kidneys are able to excrete, and how much water the kidneys hang onto)
2) Causes vasoconstriction (increases BP) (good to give in a cardiac arrest situation)
What controls ADH?
Posterior pituitary (in the brain)
What happens if you have too much ADH (Anti-Diuretic Hormone)?
Too much means hanging onto fluid
- they are not diuresing (urinating)
What happens if you have too little ADH (Anti-Diuretic Hormone)?
Too little=losing fluid
- they are diuresing (urinating)
Two things to do to see if pt has DI or SIADH
1) Look at the urine
2) Look at the serum sodium
Pancreatitis (main points)
- Acute and Chronic inflammation of the pancreas
- Causes
1) Alcoholism
2) Cholelithiasis (Gall stones), Trauma, Cystic Fibrosis – genetic link?
3) Pancreatic duct or CBD is clogged and enzymes begin to attack-Auto-digestion - Signs and Symptoms
1) Epigastric Pain > back
2) N/V, Fever, Tachycardia, Hypotension - Testing
- Enzymes increase in Amylase, Lipase
- Blood test would should Hyperglycemia because the pancreas is responsible for the production of insulin
- CT
Pancreas releases lipase and amylase into blood when they get hurt or inflamed. Both levels rise w/in 2-12 hours. Describe the levels in 3 days
Amylase levels return to normal but lipase stays elevated for up to 7-10 days helping in late diagnosis of pancreatitis
Pruritis
.
Hypothyroidism
-Decreased production thyroid hormones
-Signs and Symptoms
Childhood >
* impaired development of skeletal system and central nervous system
Children and Adults >
* Fatigue, pallor, edema, weight gain, arthralgia, cold intolerance, decreased DTR’s
* Myxedema - is edema with excessive connective tissue
* Myxedema Coma - a rare complication arising due to acute underlying Hypothyroidism and also associated to Hypoxia (low oxygen), Hypoventilation (insufficient breathing), Low Blood Pressure, Hypercapnia, low sodium and low core body temperature. It is typically treated as a life-threatening emergency.
Hashimoto’s Thyroiditis
Why is the thyroid inflamed?
Most common cause of hypothyroidism in US
Identified in 1912
Autoimmune thyroiditis
Increased F>M
Painless unilateral or bilateral enlargement of the thyroid
Testing
TSH, T3/4
Antibodies - anti-thyroid microsomal Ab, anti-thyroglobulin
-The thyroid is inflamed because there is an auto-antibody attacking the thyroid gland itself (primary problem) EXAM
Primary problem start at thyroid gland t3/t4 low
What are the 3 different hypothyroidism pathologies?
1) Hashimoto’s thyroiditis
2) Iodine deficiency
3) Subacute DeQuervains Thyroditis
Causes of hypothroidism
- Most common dysfunction of thyroid; greater in women
- Autoimmune disease
- Lack of intake - iodine
- Surgery
- Ablation
- Thyroidectomy
- Radiation: or older people, or x-rays taken at dentist, or if someone has a tumor
- Medications - hyperactive thyroid meds
- PTU – Propylthiouracil – used to treat Hyperthyroidism
- KI – Potassium Iodine
- Lithium – used to treat Bipolar Disorder. Side effects of lithium=sending someone into a hypothyroid state
McBurney’s point
Appendicitis
Parietal peritoneum –
Visceral peritoneum –
Parietal peritoneum – lines inner surfaces of body wall
Visceral peritoneum – covers organs
The Ureters
- Are a pair of muscular tubes
- Extend from kidneys to urinary bladder
- Begin at renal pelvis
- Are retroperitoneal, attached to posterior abdominal wall
- Penetrate posterior wall of the urinary bladder
- Ureteral openings are slit-like rather than rounded
- Shape helps prevent backflow of urine when urinary bladder contracts
Peristaltic contractions
Begin at renal pelvis
Sweep along ureter
Force urine toward urinary bladder
Every 30 seconds
Nephrolithiasis: Stones that are too large to pass may require surgical treatment including:
1) Using a ureteroscope to go up and snare the stone
2) Using a nephroscope to crush the stone and retrieve it
3) Using shock wave lithotripsy where a person is submerged in water containing shock waves to pulverize the stones
Treatment for gout
- Diet changes
- Decrease foods high in purines
- Beer
- ↓ Shellfish, Organ meat, Sweetbreads
- Decrease weight
- Anti-inflammatories, drugs to reduce uric acid
- Surgery-rare
Osteoarthritis
- Degeneration of cartilage
- ‘wear and tear’ disease
- Causes
- Age, Overweight, Overuse, secondary to trauma
- Articular cartilage is lost
- S/S
- Pain > mc: Hands, Wrists, Knees, Feet
- Morning Stiffness
- Pain increases with use and decreases with rest
- No systemic s/s
- Testing
- DDX: Blood test: Rheumatoid Factor
- X-Ray
- Synovial fluid aspiration – check fluid
- Tx
- Rest
- PT to help maintain ROM
- Anti-inflammatories
- Chondroitin and Glucosamine: Shown some success
Osteopenia - Osteoporosis
- Reduction in bone mass
- Causes
- Age, Malignancy
Hormonal Estrogen, Hyperparathyroidism
Chronic Renal Failure
S/S
Compression Fractures
Testing
Bone Density Scan
Next slide
X-Ray
Tx
Exercise
Ca and Vit. D Supplements
Hormone replacement
- Age, Malignancy
Coagulative necrosis
Occurs primarily in the kidneys, heart, and adrenal glands, commonly results from hypoxia caused by severe ischemia or hypoxia caused by chemical injury, especially ingestion of mercuric chloride
-Coagulation is caused by protein denaturation, which causes the protein albumin to change from a gelatinous, transparent state to a firm, opaque (not able to see through) state
Liquefactive necrosis
Commonly results from ischemic injury to neurons and glial cells in the brain. Dead brain tissue is readily affected by liquefactive necrosis because brain cells are rich in digestive hydrolytic enzymes and lipids and the brain contains little connective tissue.
- Cells are digested by their own hydrolases, so the tissue becomes soft, liquefies, and segregates from healthy tissue, forming cysts.
- This can be caused by bacterial infection, especially Staphylococci, streptococci, and Escherichia coli
Caseous necrosis
Usually results from tuberculosis pulmonary infection, especially by Mycobacterium tuberculosis. It is a combination of coagulative & liquefactive necrosis
-The dead cells disintegrate, but the debris is not completely digested by the hydrolases. Tissues resemble clumped cheese in that they are soft and granular. A granulomatous inflammatory wall encloses areas of caseous necrosis
fat necrosis
- Cellular dissolution caused by powerful enzymes, called lipases, that occur in the breast, pancreas, and other abdominal structures
- lipases break down triglycerides, releasing free fatty acids that then combine w/calcium, Mg, and Na ions, creating soaps (saponification). The necrotic tissue appears opaque and chalk-white
Gangrenous necrosis
Refers to death of a tissue and results from sever hypoxic injury, commonly occurring because of arteriosclerosis, or blockage, of major arteries, particularly those in the lower leg
- w/hypoxic & subsequent bacterial invasion, the tissues can undergo necrosis
- Dry gangrene is usually the result of coagulative necrosis
- The skin becomes very dry and shrinks resulting in wrinkles, and its color changes to dark brown or black
To get angina
Vasospasm=?
Thrombosis:
Vasospasm=variant
Thrombosis: unstable
How to get heart to contract with more force:
fight or flight response
How to get blood pressure to increase?
exercise, increase sodium intake, caffine, certain drugs, genetics (essential hypertension)
If you block ACE you make less?
ADH
Angiotensin II does what?
Constricts blood vessels and raises blood pressure
An ACE inhibitor lowers the?
Amount of work the heart has to do
ACE (Angiotensin-Converting Enzymez) function
Used to treat congestive heart failure, high blood pressure, and many other medical conditions.
- It causes the blood vessels to become dilated (enlarged) thus causing a reduction in BP
- This lowering of BP makes it easier for the heart to pump blood and it can improve the function of a failing heart
What happens when blood pressure falls too low?
1) Kidneys release renin into the blood stream
2) Renin reacts with the protein called angiotensinogen produced by the liver
3) As a result they form angiotensin I
4) Another reaction converts angiotensin I to angiotensin II with the help of angiotensin converting enzyme (ACE) found in the respiratory system
- Angiotensin II is a powerful substance that circulates around the body in the blood stream & induces several changes on the cardiovascular system: such as stimulating adrenal cortex to release aldosterone & constricting the blood vessels around the body
- aldosterone increases the reabsorption of water & sodium into tubules of kidneys, as a result the volume of blood & the concentration of salt in the blood increases leading to high BP
- the constriction of blood vessels & high pressure inside the vessels also means an increase in BP. Both of these events cause the heart to exert more pressure while pumping blood into the main arteries, hence it reverses the low BP
- It can also lead to other cardiovascular disorders if it persists for a long time
Ace inhibitors
Reduces the impact of RAS (renin angiotensin aldosterone system) on the BP by inhibiting the angiotensin converting enzyme (ACE). As a result the conversion of angiotensin I to II is slowed down which brings about several changes int he cardiovascular system
-The rate of water reabsorbs in the kidney drops and so blood volume decreases & blood vessels are relaxed and
become dilated
- Both of these factors reduce the work load on the heart, it thus reduces the BP & enhances the capacity of the heart
Beta blockers definition
Beta Andrenergic blocking agents. They are medications that are used in many different heart diseases including: elevated BP, arrythmias, cardiomyopathy, heart failure, angina pectoris (chest pain)
Mechanism of beta blockers
Our brain produces chemicals called neurotransmitters these are chemicals that transmit a signal across a synapses from one neuron to another
- each neurotransmitter activates or stimulates a specific receptor. To successfully transmit a signal from one neuron to another cell similarly a key fitting into a lock
- certain transmitters called catecholamines (norepinephrine, epinephrine) are released from nerve endings at the sympathetic nervous system (involuntary nerve network that enables the body to withstand stress, anxiety, and exercise). This stimulates receptors known as adrenergic receptors
- one catecholamines bind to adrenergic receptors this chemical creates the fight or flight response which includes: increase in HR, heart muscle contractions, BP, and relaxation of the smooth muscles in the bronchiole tubes in the lungs making it easier to exercise and expand the lungs
- there are two types of adrenergic receptors: alpha and beta
- Beta blockers work by blocking the neurotransmitters catecholamines (norepinephrine, epinephrine) from binding to the beta adrenergic receptors
- there are 3 known types of beta receptors and they control several diff functions based on their location: beta 1 (heart, kidney), Beta 2: lungs, liver, vascular smooth muscle, skeletal muscle), beta 3 (fat cells)
- when beta blocking drugs are given through mouth or IV they inhibit the normal sympathetic effect that acts through the receptors. By doing so the HR, and BP are reduced & the heart will pump with less intensity this in turn will reduce the O2 needs of the heart
- they modify heart’s stress don’t eliminate
All ACE inhibitors end in?
Action?
Effects?
- Pril
- Decrease perihperal vascular resistance without: increasing cardiac output, increasing cardiac rate, increasing cardiac contractility
- Effects: Dizziness, orthostatic hypotension, GI distress, Non-productive cough, HA
Beta blockers end in?
Olol
Calcium channel blockers
In the body the concentration of calcium outside the cell is several thousand much higher than that inside the cell
- cells have Ca+ channels embedded in its membrane which opens to let Ca+ go into the cell once stimulated
- Some cells have L type voltage gated channels located on vascular smooth muscle, cardiac myocytes, cardiac nodule tissue
- these blockers prevent or reduce the opening of these channels
- there are diff classes of Ca+ channel blockers but almost all act on the L type voltage gated Ca+ channel therefore blocking or reducing Ca+ entry into the cells means inhibiting the Ca+ influx and thus causes vasodilation
- by acting on the vascular smooth muscle Ca+ channel blockers reduces the contraction of the arteries which causes an increase in arterial diameter
- this drug primarily affects the arteries with minimal effects on venous vessels
- they also have a negative inotropic effect by acting on cardiac muscle. They reduce the force of contraction in the heart
- also have a negative chromotropic effect by slowing down the induction of the electrical activity w/in the heart therefore may effect the heart beat
- also can exhite a negative dromotropic effect by slowing down the conduction of the electrical activity in the heart thus the conduction of velocity also decreases at arterial ventricular node which can slow HR
- Used to treat high BP, chest pain, tachyarrythmia
non-STEMI – indicates?
subendocardial MI
STEMI – indicates?
transmural MI
If someone’s left heart is dying blood is coming from the?
If someone’s left heart is dying blood is coming from the lungs and it backs up from the lungs the fluid in the tiny capillaries goes to the lungs.
If you percus someone lungs it will be dense, sound dull
What are the lab values for a MI after it happened?
Increase of Troponin I & T: lasts one week
Increase CK or CK-MB: lasts 48 hours
Increase myoglobin: lasts 24 hours
ASIS-Anterior superior illiac spine is where you will find the?
McBurney’s point
Colon cancer can compromise wall…
s/s lower blood pressure.
When capillaries become leaky you lose fluid
Blood pressure down HR up to compensate
BC=Blood culture, checking for bacteria in the blood. If you know what bacteria is in the blood you will know what medication to give PT.
Peritonitis
Etiology unknown
Risk factor: dehydration, things high in oxalate acid (coffee, chocolate, blueberries)
What hormone causes you to calcitrial
Other hormone that raises what? PTH from parathyroid glands
s/s might have fever as well
Blood in urine can come from where?
BUN=Blood, urea, nitrogen
Clinically creatinine is normally not effected by?
Check their PH level as well
Nephrolithiasis
Rheumatoid Arthritis
- Autoimmune Joint Inflammation
- Adult
- Juvenile > limp, high fever, Hepatosplenomegaly (HSM)
- Causes
- F>M, age, hereditary, Smoking
- S/S
- Inflammed joints > Wrists, PIP’s, MCP’s, Elbow, Knee, Ankle, MTP’s
- Decreased motor strength
- Fever, fatigue, pericarditis and effusion, pulmonary effusion, scleritis
- Morning stiffness
- Testing
- ↑ESR and ↑CRP*, CBC, RF, X-Ray
- ESR=Erythrocyte sedimentation rate
- CRP: Where have we seen this before?
- ↑ESR and ↑CRP*, CBC, RF, X-Ray
- Tx
- No cure: ↓inflammation and pain
Sciatica
- Nerve pain with radiation
- Causes
- Nerve compression > muscular, disk, piriformis syndrome, tumors
- S/S
- Radiation of pain from lower back to buttock to lower leg
- Neuropathies ( abnormal and usually degenerative state of the nervous system or nerves)
- Parasthesias (abnormal condition in which you feel a sensation of burning, numbness, tingling, itching or prickling. Paresthesia can also be described as a pins-and-needles or skin-crawling sensation)
- weakness of the muscles
- muscle cramps in buttock or leg and diminished reflexes in knees and ankles
- Loss of bladder and bowel control
- Testing
- X-Ray, CT, MRI
Osteomyelitis
- Infection of the muscle and bone
- Causes
- Infection > Staph aureus/Pseudomonas, Metastasis
- DM pts
- S/S
- Localized to systemic infection with skin ulceration
- Bone and joint pain
- Testing
- Blood test - ↑WBCs, ↑CRP (why?) maybe also ESR increased
- Cultures > wound and blood cultures
- X-Ray, CT
- Bone scan
- Tx
- Antibiotics
- Surgical debridement
- Amputate
Cellulitis
- Bacterial skin infection
- Causes
- Staphylococcus
- Streptococcus
- Injury, Dermatitis, Insect Bites
- DM, Edema, Fungal infections, IV drug use
- S/S
- Usually seen in lower legs
- Signs of Infection > ?
- Testing
- C&S
- Second most common type of arthritis
- Seen in wrists, hands, knees, ankles, and feet
- Typically occurs at same joints on both sides of the body
- Can also affect other organs of the body such as the eyes, skin, heart, lungs, kidneys, nervous system, and digestive tract
- an auto-immune disorder (body attacks itself by mistake)
- in this disease the immune system attacks joints and organ tissues
Rheumatoid arthritis
Chronic, systemic, inflammatory autoimmune disease distinguished by joint swelling and tenderness and destruction of synovial joints leading to disability and premature death
Rheumatoid arthritis (RA)
This disease can cause
1) inflammation
2) destruction of joints
3) fever
4) malaise
5) rash
6) lymph node or spleen enlargement
7) Raynaud phenomenon (transient lack of circulation to the fingertips and toes)
8) fatique
9) weakness
10) anorexia/weight loss
11) generalized aching/stiffness
Rheumatoid arthritis
Blood flow in the heart
- Deoxygenated blood goes into the superior vena cava to the R atrium as well as from the inferior vena cava
- From R atrium it goes down the tricuspid valve to the R ventricle
- R ventricle is going to contract and then shoot through the pulmonary valve to the pulmonary arteries to go to the lungs to pick up O2
- then the blood is going to return to the heart through the pulmonary veins to the L atrium down through the mitral valve (bicuspid valve) to the L ventricle
- L ventricle is going to contract and blood will go through aortic valve and out through the aorta to the body
What happens if the R ventricle is not contracting effectively?
There will be a decrease amount of blood that makes it to the lungs and we will have a back up of blood through the R atrium
- Back up of blood to the body
- Decrease amount of blood to the lungs
- JVD (Jugular vein distention
- edema
R sided heart failure
what happens in L sided heart failure if the ventricle doesn’t contract with as much force?
- Not enough blood will be able to get out to the body
- if ventricle can’t squeeze effectively then all the blood coming from L atrium will start to back up to the lungs
- If you hear lung sounds you will hear crackles due to excess fluid
- Decrease amount of blood out to the body (this is O2 rich blood which we need for our tissues)
- due to low O2 they will be fatigued/tired
- Decrease pulse
- Decrease perfusion
- crackle sounds in lung
- dysnpnea
L sided heart failure
Ascites
Accumulation of protein-containing fluid in peritoneal space
Portal HTN
Diabetes Insipidus
- Lack of ADH
- Causes
- Neurogenic - absence of ADH (Pituitary problem?)
- Nephrogenic - inadequate response of renal tubules to ADH
- Psychogenic - excessive fluid intake that suppresses ADH
- Signs and Symptoms
- Excessive urination and thirst
- Polyuria and polydipsia
- Excretion of large volume dilute urine, dehydration
- Testing
- ↑Serum osmolarity vs. ↓Urine osmolarity
- Plasma ADH levels
S/S
- Up to 20L Urine/day
- Decrease Specific gravity
- Decrease osmolarity
- Hypoedema
- Increase thirst
- Tachycardia
- Decrease BP
Diabetes Insipidus
Congestive heart failure
- Decreased pumping ability of the heart to meet demands of tissue - ↓CO, pooling in venous system/organs
- L sided
- R sided
- Systolic or diastolic
- Causes
- Atherosclerosis > CAD
- HTN, valvular disorders, arrhythmias, anemia, MI
- S/S
- Fatigue, weakness, dyspnea, orthopnea, pink frothy sputum, cough, edema
- Testing
- BNP, CXR, EKG, Echocardiogram, Ejection Fraction
The hearts pumping power is abnormal. Blood moves through the heart at a slower rate and the pressure in the heart increases therefore the heart becomes congested. As a result the heart cannot pump enough O2 to meet the body’s demand.
- Can be divided into: L sided heart failure or R sided heart failure
- Can be either from: systolic dysfunction (inability of heart to contract and push out the blood), or diastolic dysfunction (inability of heart to relax)
- Risk factors:
1) CAD
2) MI
3) Cigarette smoking
4) Hypertension (HTN): leads to L ventricle hypertrophy which makes it harder to oxygenate the heart muscles
5) Obesity
6) Diabetes
7) heart valve disease (e.g Aortic stenosis)
8) Cardiomyopathy “heart muscle disease”- dilated cardiomyopathy, hearts ability to pump blood is decreased because the hearts chambers are dilated
- hypertrophic cardiomyopathy: Thickening of the heart muscle
- Restrictive cardiomyopathy: walls of the heart are abnormally rigid & lack flexibility to expand
.
Congested heart failure S/S Dilated pupils, a sympathetic nervous system response= Skin pale, gray, or cyanotic= Dyspnea, SOBOE, is early symptom from pulmonary congestion = Orthopnea cannot break unless sitting up= Crackles, wheeze= Cough frothy pink or white sputrum= Decreased bp= N/V= ASCITIES= DEPENDENT PITTING EDEMA= ANXIETY= FALLING 02= CONFUSTION= JUGULAR= INFARCT= FATIQUE= S3 GALLOP, TACHYCARDIA= ENLARGED SPLEEN & LIVER= DECREASED URINE OUTPUT= WEAK,PULSE COOL MOIST SKIN=
Some S/S due to left some due to R and know what ones are Dilated pupils=both Skin pale, gray, or cyanotic=L Dyspnea, SOBOE=L Orthopnea=L Crackles, wheeze=L Cough=l dECREASED bp=L N/V=R ASCITIES=R DEPENDENT PITTING EDEMA=R ANXIETY=L FALLING 02=L CONFUSTION=L JUGULAR=R INFARCT=L FATIQUE=L S3 GALLOP, TACHYCARDIA=BOTH ENLARGED SPLEEN & LIVER=R DECREASED URINE OUTPUT=L WEAK,PULSE COOL MOIST SKIN=L
Any issue with the lungs that causes the R side heart to fail is called?
cor pulmonale
Addison’s disease
- Decreased Adrenal Function
- Causes
- Primary adrenal insuff. – Infection (TB), tumor, hemorrhage; ↓ cortisol & often aldosterone
- NOT Secondary adrenal insuff. – Pituitary insufficiency
- S/S
- Electrolyte Imbalances – Weakness, fatigue, hypoglycemia, hypotension, N/V, hyperpigmentation
- Addisonian Crisis - severe acute adrenal insufficiency: low BP, low glucose, hyperkalemia
- Testing
- ACTH, ACTH Stimulation test (inject ACTH and check Cortisol levels), CT/MRI
TB can lead to?
Addison’s disease
NASH – Nonalcoholic Steatohepatitis
Fat deposition in the liver that causes inflammation and damage 1-2% of Americans Cause: Idiopathic S/S ‘Silent’ liver disease May take decades to progress – gradual Dull abdominal pain Jaundice - when more when advanced to liver failure Fatigue Testing Elevated ALT - alanine aminotransferase Elevated AST - aspartate aminotransferase Biopsy to determine for cirrhosis Ultrasound picks up fatty liver
Cirrhosis
- Characterized by fibrosis of liver and regenerative parenchymal nodules
- Causes
- EtOH, Hepatitis B and C, Bile Duct Obstruction
- Nonalcoholic Steatohepatitis (NASH) - fat, inflammation, damage.
- Assoc. w/obesity, increased blood lipids, insulin resistance
- Signs and Symptoms
- Fatigue, N/V, Edema, Jaundice, GI Bleeding, Pruritis
Portal Hypertension > Ascites, Esophageal Varicies
Bleeding disorders, hypoglycemia, encephalopathy
- Fatigue, N/V, Edema, Jaundice, GI Bleeding, Pruritis
- Testing
- ↑ALT, AST, Bilirubin, CT/MRI
Liver Biopsy
S/S
- ‘Silent’ liver disease
- May take decades to progress – gradual
- Dull abdominal pain
- Jaundice - when more when advanced to liver failure
- Fatigue
NASH – Nonalcoholic Steatohepatitis
This disease is associated with obesity (including obese children), high levels of cholesterol and triglycerides, metabolic syndrome, and type 2 diabetes mellitus and is the most common chronic liver disease in the US
Nonalcoholic fatty liver disease (NAFLD)
Some individuals with NAFLD will develop nonalcoholic steatohepatitis (NASH) with?
hepatocellular injury, inflammation and fibrosis. Usually asymptomatic and may remain undetected for years. Most severe forms progress to cirrhosis and end-stage liver disease
S/S of anemias
Fatigue/Weakness/Dizzy Pallor SOB/Dyspnea Chest pain/Arrhythmias/Tachycardia Orthostatic hypotension or syncope Cold hands and feet Nail changes Decreased growth and development Neurological S/S (Vitamin B12 deficiency) Mild anemia may only cause S/S during exertion due to compensation
Anemia of acute blood loss
- Bleeding
- Trauma, peptic ulcer, hemorrhoids, GI bleed
- Hct (% FORMED ELEMENTS BY VOLUME) is low due to hemodilution - shift of fluid from the interstitial space into circulation to compensate for blood loss
- Normocytic, Normochromic anemia
Production of \_\_EPO\_\_ by the kidneys Increased reticulocyte (immature RBC’s) count after 1 week
Anemia of chronic blood loss
Rate of loss exceeds ability to regenerate
Iron reserves become depleted iron deficiency occurs
Occult blood loss can take months to cause anemia
Microcytic, hypochromic anemia
MCV? MCH?
Low and Low
Megaloblastic anemias (Macrocytic-Normochromic)
1) Pernicious anemia (PA): Most common type of macrocytic anemia, is caused by vitamin B12 deficiency
2) Folate (folate acid) B9 deficiency
Microcytic-Hypochromic anemias
1) Iron deficiency anemia (IDA)
2) Chronic diseases
Normocytic-normochromic
1) Aplastic
2) Hemolytic
S/S for aplastic anemia
Fatigue Shortness of breath with exertion Rapid or irregular heart rate Pale skin Frequent or prolonged infections Unexplained or easy bruising Nosebleeds and bleeding gums Prolonged bleeding from cuts Skin rash Dizziness Headache
Subacute De Quervain’s Thyroiditis
Inflammation of thyroid Causes Viral URI S/S Neck pain Viral S/S Transient hyperthyroidism (4-10 weeks) followed by transient asymptomatic hypothyroidism (2 months) No myxedema Complete recovery Testing: Anti-thyroid Ab negative
Valvular Defects
- Dysfunction of the heart valves
- Stenosis: valve doesn’t open fully
- Regurgitation/Insufficiency: valve doesn’t close fully
- Causes
- Mitral valve stenosis - Rheumatic fever
- Aortic valve stenosis - congenital or acquired, RHD
- Tricuspid valve regurgitation - R ventricular dilation & failure, usually secondary to pulmonary HTN
- Mitral valve regurgitation - MV prolapse, infective endocarditis, MI, CT (Connective Tissue) disease
- S/S
- Heart murmur, chest pain, cough, dyspnea, orthopnea, palpitations
- Testing
- Chest X-ray, EKG, Echocardiogram, TEE-see next slide
Mitral valve prolapse
- Common in young women
- Caused by changes in connective tissue of leaflets:
one or both mitral leaflets are enlarged, hooded, floppy, and prolapse/balloon back into LA during systole
Regurg when ballooning allows blood to leak back into LA
Left atrial hypertension and dilation, stretches valve causing further backflow - Causes: genetic, connective tissue disorder, hyperthyroidism
- S/S: usually asymptomatic and no treatment required; palpitations, fatigue, dyspnea, angina, depression, anxiety
- Prognosis overall very good
Complications: increased risk of infective endocarditis, arrhythmia, mitral regurgitation
Cardiomyopathy
Diseases of myocardium (next slide) Hypertrophic Dilated Restrictive Causes HTN, valvular defects, hyperthyroid, Thiamine (B1) def, EtOH, drug use S/S Dyspnea on exertion or rest, dizziness, edema, arrhythmias, palpitations Testing EKG, Echocardiogram, Chest X-ray, BNP
Dilated (congestive) cardiomyopathy
All four chambers are dilated. Idiopathy or drug toxicity/chronic alcoholism, end-stage viral myocarditis, familial
Hypertrophic cardiomyopathy
LV & septal hypertrophy, LA dilated, impaired diastolic filling. Reduced SV, dyspnea. Familial hypertrophic cardiomyopathy (FHC)
Restrictive cardiomyopathy
Fibrosis of cardiac muscle results in impaired ventricular filling. Biatrial dilation. Most common causes are amyloidosis & hemochromatosis
Hypothyroidism Iodine deficiency
Not enough iodine in the diet (iodine deficiency) – WHAT TYPE OF HYPOTHYROIDISM WOULD THIS BE? Primary, secondary, or tertiary? Not enough iodine=primary problem
Causes swelling of the thyroid gland
Leads to a decreased metabolic rate, weight gain, fatigue, depression, lower body temp.
