Final Blueprint-Summer 2024 Flashcards
Risks for prostate cancer (What is it NOT?)
It IS: MC dx of non-skin cancer
6th leading cause of death
Path: uncontrolled growth of prostate gland cells
R/F:
age, family history, obesity, taller/heavier at birth, MC in African American males, Genes: BRCA1 and BRCA 2; increased hormone IGF1, pesticides
S/S: asymp. until advanced
DX: exam and DRE
TX: prostatectomy, TURP, radiation, chemo/immuno
Digital Rectal exam (DRE)
Assessing the prostate gland. It should be firm, not soft or enlarged.
Anatomically: ANTERIOR surface of the prostate through the rectal wall.
Epididymitis physical exam findings and what relation to STI’s (maybe a scenario question)
What is a PREHN sign?
Inflammation of the epididymis (coiled tube behind testicle)
Tenderness and swelling of epididymis.
+ Prehn sign (pain relief when the affected testicle is elevated)
*NOT low back pain , abd pain , or Cremasteric reflex
NOT impotenence, anal cancer, or uti
acute epidydmitis c/b infection:
STD’sEverytime you hear epididymitis, think STD’s
Gonorrhea and chlamydia
Peyronie’s disease- What is it?
Fibrosis and scarring of the sheath around the corpora cavernosa (erectile tissue in the penis)
R/F: fam hx: connective tissue ds, age (45-70y)
o Painful bent erection that can lead to erectile dysfunction.
S/S: Plaque bands under penis, curved penis,
Dx: exam, U/S while erect
Tx: Penile traction, surgery, meds: collagenase clostridium histolyticum, verapamil, interferon
Priapism- What is it? (maybe a scenario question)
An involuntary, prolonged and painful erection, not asso. w/ sexual arrousal >4hrs
(priapism or scrotal pain (possible torsion) send to ER)
Urologic emergency
60% idiopathic
Asso. w/: spinal cord trauma, sickle cell, leukemia, pelvic tumors, or trauma, or cocaine use
TX: ice packs to perineum, iced enemas, needle aspiration of dorsal glans
Phenylepherine to constrict blood vessels, ketamine infusion, spinal anesthesia
BPH symptoms (probably a question of “What is NOT a symptom?)
What is considered a large prostate? >80gms
When it obstructs the urine flow significantly by hypertrophied.
o Symptoms: frequent urinating, weak stream, nocturia, urinary retention
Dx: DRE (larger than walnut and frim), UA, PSA, urine flow, PVR, U/S, Bx, cysto.
o Normal size prostate: 20-25 g and 30-40 ml
Exam: enlarged prostate and hard on palpation
Obliterated median sulcus
Risk factors for bacterial prostatitis
(will have to answer what is NOT a risk factor on exam)
P: infection of prostate:
MC: enterobacteriacaeae
s/s: enlarged prostate, infection signs
Young middle-aged male
Previous prostatitis
UTIs
Recent prostate procedures (biopsy)
Unprotected sex
HIV infection or AIDS
Catheter use
P: Ascending UTI
Testicular cancer-basic understanding
Overgrowth of germ cells in testes
s/s: bump, heaviness in scrotum, lower belly dull ache, scrotal pain/swell.
Relatively rare but highly treatable
Is often curable, especially when detected early
Young men (15-35 years old)
Risk factors
Family history
high androgen levels
Cryptorchidism (Undescended testicles)
Certain genetic conditions
age, obesity, testicular stones
TX: surgery (orchidectomy)
Testicular torsion- Surgical emergency (What would you do for this?)
o Occurs with twisting of the spermatic cords and compromise blood flow.
o Sudden pain and swelling of the testicle.
Medical emergency
Neg Phrens sign
R/F: age 12-18; prev & fam hx
o Immediate surgical detorsion to restore blood flow to the affected testicle.
ADH role- vasopressin- is produced by the hypothalamus and released by the posterior pituitary gland.
o Its primary role is to regulate water balance in the body by controlling water reabsorption in the kidneys.
o ADH acts on the renal collecting ducts, increasing permeability to water, leading to more water being reabsorbed from the renal tubules back into the bloodstream causing concentrated urine.
o Released when osmolality is increased and volume in the blood stream is decreased.
Most common cause of ADH overproduction-ectopic production
SIADH (can be caused by tumors on the pituitary)
=severe hypoNA-cerebral edema-sever neuro damage)
o In SIADH, the body produces excess ADH even when the plasma osmolality is low.
-small cell lung cancer
Endocrine system specializes in secreting substances in three categories…
o Endocrine- affects distant cells- travel through the blood, often called hormones
o Autocrine- affects cells that produce it
o Paracrine- affects nearby cells
Hypothyroidism
o Iodine deficiency is the MC cause worldwide
o Hashimoto’s disease is the MC type in the US
AKA: Autoimmune thyroiditis
o Symptoms: fatigue, weight gain, cold intolerance, goiter, dry skin, puffy face, thin hair, poor memory
R/F: surgery, radiation to area, lithium, female, family hx, T1DM, celiac
Dx: TSH high and T4 low
Comp: Myxedema coma- ER
Normal glucose and insulin homeostasis
Glucose production occurs in the liver (gluconeogenesis) and utilized by peripheral tissues.
o When glucose is in fat cells its stored in lipids which inhibits glycolysis, lipolysis, and proteinalysis.
o When glucose is in muscle cells, it becomes glycogen or it oxidizes, forming ATP for energy sources for all organs.
o The primary function of insulin is to increase the uptake of glucose in the muscle and fat cells, maintaining blood glucose levels
Insulin increases the uptake of glucose-apply to homeostasis
Parathyroid hormone does what? (Produced by parathyroid glands)
Increases serum calcium concertation by stimulating bone reabsorption.
Enhances renal tubule reabsorption of calcium.
Decreases serum phoshate levels
Antagonist of Calcitonin
Promotes activation of vitamin D, which aids in calcium reabsorption from the intestine.
Grave’s disease presentation
The MC cause of hyperthyroidism
o Key features:
It affects 7x more women than men in US, >30yo
Autoimmune disorder with antibodies targeting the thyroid-stimulating hormone receptor.
Clinical manifestation: weight loss, palpitations, ophthalmopathy (vision changes), exophthalmos (bulging eyes), and goiter, anxiety, tremor, heat sensitive, fatigue, thick/discolor skin
Dx: autoantibodies and opthalmic changes, thyroid levels, radioactive iodine uptake,
COMP: Thyroid storm
Type 2 DM (True or False) statements)
o Often silent initially (asymptomatic).
o Combination of insulin resistance (peripheral tissues) and relative insulin deficiency (obesity makes pt more prone to insulin resistance).
o Increased glucagon levels lead to hepatic glucose production and beta cell mass and fuction.
o Common symptoms:
Polydipsia- excessive thirst
Polyuria- excessive urinating
Polyphagia- excessive eating
R/F: obesity, fat stored in and, fam hx, low HDL, High triglycerides, age >35y, predm, gest dm, polycystic ovarian (PCOS)
Dx: A1c 6.5%+ x2, random glu >200, fasting >126
Diabetes Insipidus-
ds of posterior pituitary
-Insufficient ADH activity leads to polyuria and polydipsia.
3 forms: neurogenic or central di, nephrogenic di, primary polydipsia or excessive thirst appreciation.
neurogenic or central DI- insufficient secretion of ADH.
-Occurs when any organic lesion of the hypothalamus, pituitary stalk, or posterior pituitary interferes with ADH synthesis, transport, or release.
-Causative lesions include primary brain tumors, TBI, hypophysectomy, aneurysms, thrombosis, infections, and immunological disorders. Genetics.
nephrogenic DI- inadequate response of the renal tubules to ADH.
-caused by disorders and drugs that damage the renal tubules.
-Can include pyelonephritis, amyloidosis, destructive uropathies, and polycystic kidney disease. -Drugs can affect include lithium, colchicine, amphotericin B, loop diuretics, and general anesthesia. Genetics.
Type 1 DM
○ Pathophysiology: Type 1 DM is an autoimmune disorder where the immune system attacks and destroys pancreatic beta cells. This leads to insulin deficiency.
○ Clinical Notes: Patients with type 1 DM require exogenous insulin for survival.
R/F: fam hx, age (4-7 & 10-14 yo)
Polydipsia=
excessive thirst
Polyphagia=?
Excessive eating
Polyuria=?
excessive urination
Diagnosis of DM requires what findings?**
oFast plasma glucose of ≥ 126 mg/dL
o HbA1c ≥ 6.5%
o Random plasma glucose ≥ 200 mg/dL with symptoms.
o Oral glucose tolerance test (OGTT) with 2-hour plasma glucose ≥ 200 mg/dL.
A high carbohydrate diet with high insulin response is still associated with glycation damage even if no diabetes occurs. If you have a patient who is eating horribly, it is still something that is damaging even if they don’t have diabetes.
Diabetes is also associated with an increased risk of damage to kidneys, eyes, nerves, and blood vessels due to the glycation process. It is the leading cause of end stage renal disease, adult onset blindness, Lower extremity amputations. It is
NOT a single disease but a group of diseases that all involve hyperglycemia
Cushing syndrome (scenario)
o Cushing syndrome results from chronic exposure to excess cortisol (e.g., due to adrenal tumors or corticosteroid use). It leads to metabolic disturbances, hypertension, and muscle wasting.
**Define: overproduction of pituitary ACTH by a pituitary ademona?
Cortisol secretion and lack of ability to increase ACTH and cortisol in response to stressors?
o Presentation:
Weight gain of adipose tissue in trunk, face, and cervical areas
Truncal obesity
Moon face
Buffalo hump
Purple Striae
Bronze or brownish hyperpigmentation of the skin
Sodium and water retention, glucose intolerance, protein wasting
DKA- increased glucose demands (illness or stress) and severe insulin deficiency that results in the liver producing ketones
o Key features: hyperglycemia, ketosis, metabolic acidosis, and dehydration
s/p illness-incr adrenaline and cortisol,
s/s: thirst, freq uo, n/v, sob, fruity breath, ams
o 3 I’s that are associated
Incr glucose demand in the liver producing ketones
Infection
Ischemia
Insulin deficiency
dx: ketones, blood acidity, UA
Causes and complications of hyperglycemia
o Visual impairment leading to blindness
o Micro and macrovascular changes due to oxidative stress
o Increased risk of stroke and MI
o Nephropathy due to glomerular enlargement
o Basement membrane thickening
o ESRD
o Delayed wound healing (gangrene)
Insulin resistance (skin side effect)
Acanthosis nigricans (dark, thickened patches) due to hyperinsulinemia.
Anterior Pituitary produces 6 hormones
o Adrenocorticotropic hormone (ACTH)
o Melanocyte - stimulating hormone (MSH)
o Thyroid stimulating hormone (TSH)
o Follicle- stimulating hormone (FSH)
o Luteinizing hormone (LH)
o Growth hormone
o Prolactin
o β-Lipotropin-
fat catabolism
o β-Endorphins-pain perception
Posterior Pituitary produces 2 hormones
o Oxytocin- causes uterine contractions and milk ejection in lactating women
o ADH
SIADH causes what type of hyponatremia?
o Euvolemic hyponatremia or dilutional hyponatremia
o Clinical signs and symptoms include dilutional hyponatremia, concentrated urine, and fluid overload.
Hyponatremia: Na <135
Hypoosmolality: <280
Urine hyperosmolarity
Hypervolemia
Weight gain
Serum sodium levels: 110-115
muscle cramps, n/v, HA, balance, AMD, Seizure,Coma
R/F: age, small cell lung CA, stroke, trauma, hypopituitarism, hypothyroidism
COMP: diluted hyponatremia (ER): ams/sz/coma (ER)
Hyponatremia and volume
euvolemic hyponatremia question (SIADH)
hypovolemic
hypernatremia (excessive sweating),
hypovolemic hyponatremia (CHF, extreme volume
overload, cirrhosis where you have a swollen ascites picture)
Venous Insufficiency- How will the patient present?
Is impaired venous return leading to pooling of the blood in the vessels.
Pt will present with skin changes, brownish discoloration of the skin, leg swelling and varicose veins, ulcers, or RLS
R/F: obesity, pregnancy, fam hx, injury to lim, sit/stand prolonged, smoking, DVT, phlebitis
Dx: Duplex U/S
HTN Emergency- vs urgency
severe high blood pressure leading to end- organ damage with systolic BP >180 and diastolic BP > 120 ; with organ damage
o With urgency there are not exacerbated signs and symptoms, and not yet organ damage
o Pt will present with sequela such as, neurologic changes (encephalopathy), renal failure, cardiac disease (CHF, and CAD), retinal changes
o Rapid BP reduction is necessary to restore blood flow and oxygenation
STEMI- complete occlusion of the coronary arteries leading to myocardial ischemia and necrosis.
EKG- ST elevation in specific leads
Anterior: LAD artery
Inf/Lat: RCA/LCX artery
s/s: angina, SOA, N, Palp, anx, sweating, dizzy, radiating pan
R/F: poor life choices
EKG
Inferior: II, III, AVF
Septal: V1, V2
Anterior: V3, V4
Lateral: I, AVL, V5, V6
Risk factors for DVT
o Immobility
o Surgery
o Virchow’s Traid
Hypercoagulability of blood
Impaired venous blood flow (stasis)
Vessel injury/ endothelial damage
AMI & Location of MI diagnostic test
o Results from coronary artery occlusion
MC cause: coronary atherosclerosis
o ECG- shows the location of damage (anterior, inferior or lateral)
o Troponin level (elevated) and EKG findings guide diagnosis
What is the most important tool to assess for myocardial damage? (Will have ekg that’s obvious)
EKG
If you have ST elevation it is most likely to go with pericarditis.
ST depression is not
necessarily a STEMI because STEMI shows big ST elevation changes.
ACS presentation
o Unstable angina and MI resulting from atherosclerotic plaque rupture and thrombus formation
o Presentation: chest pain, EKG changes, and cardiac enzyme aid in diagnosis
transient murmur, new onset pulm crackles, hypotensive,
But if they tell you that this pain is reproduced with
palpitation it is not acute coronary symptoms. Basic angina. If the chest pain because they have been coughing too much? Is it from another disease process? Pain that is reproducible is NOT ACS
CAD presentation
Angina: chest pain, pressure or tightness, squeeze or ache
soa
fatigue
nausea
lightheaded
heartburn
cold sweats
r/f: OSA, hi CRP, hi trigly., preeclampsia, RA, lupus, age, male, smoking, HTN, HLD, DM, Obesity, unhealthy die, ETOH
Venous stasis ulcers are due to what?
Impaired blood & lymph return, leading to tissue hypoxia and skin breakdown. increased pressure and fluid backup
R/F: age >55, obesity, PE, DVT, preg,, inactivity
Compression therapy and wound care for treatment
NSTEMI versus Unstable Angina is determined by what test?
**Troponin elevation is seen in NSTEMI
transient ST elevation
ST depression
New T wave inversion
Purkinje fibers- (heart pace)
specialized cardiac muscle fibers that conduct electrical impulses rapidly, ensuring coordinated ventricular contraction. Dysfunction can lead to arrhythmias.
o 20- 40 (kicks in when SA and AV nodes fail)
o SA node: 60-100 bpm (located in the right atrium)
o AV node: 40- 60 bpm
AAA (abdominal aortic aneurysm) presentation
o Pathological dilation of the abdominal aorta
o Will present with: HTN
Abd pain, often radiating to the low back
Pulsatile abdominal mass *** (dead give away)
Disection or rupture= ER! ER!
Raynaud’s phenomenon- (risk factors)
vasospasms of digital arteries leading to color changes (pallor, cyanosis, erythema) in response to cold or stress.
o Risk factors
Cold exposure
Stress
Smoking
Female gender
Connective tissue disease
atherosclerosis, carpal tunnel syndrome,
age 15-30 years
familiy hx
Cardiogenic shock signs of inadequate tissue perfusion
Sudden s/s
tachy, soa, LOC, weak pulse, cold extremities, pale skin
o Oliguria***- reduces urine output due to poor organ perfusion
Pulmonary congestion
o Hypotension
o Cool extremities
o Altered mental status
HF presentation and diagnostics- due to impaired cardiac function (scenario question). VS. STEMI
Presentation is dyspnea (shortness of breath), fluid retention and fatigue.
irreg HR, Wheeze, cough, CP
o **Laboratory- BNP levels (B- type natriuretic peptide) <100 picos/mL
The most appropriate diagnostic test- Echocardiogram
cardiac markers
EF >50%=preserved LV fin
Risk Factors for DVTs (don’t get distracted by the distractors)
obesity,
pregnant/1st six weeks postpartum,
family history of DVT,
recent surgery or injury to a deep vein,
taking birth control pills or receiving hormone therapy, seated for long plane/car ride, smoking tobacco,
recent lower extremity fracture,
older age,
recent or recurrent cancer,
CVC placement,
prolonged immobility,
varicose veins
Blood flow pattern through the valves of the heart (just 1 question)
o Right atrium → tricuspid valve → right ventricle → pulmonary valve →pulmonary artery → lungs
o Left atrium → mitral valve → left ventricle → aortic valve → aorta → systemic circulation
The anterior wall of the heart is oxygenated by which coronary artery?
Left anterior descending artery (LAD) supplies the anterior wall of the heart
Circumflex wraps around the side
Right coronary artery supplies the right side of the heart
Myocardium oxygen extraction
o Extracts oxygen from coronary blood flow during diastole to meet metabolic demands.
o Reduced oxygen supply can lead to ischemia
What is the most common cause of an MI?
o Coronary atherosclerosis (scenario question)
o Women present differently- how will she present?
o S/S
Severe, sudden chest pain
Pain radiating to neck, back, shoulders, jaw and arms
Unrelenting indigestion
Nauseous and vomiting
o EKG changes
o Cardiac markers are elevated
Mechanisms of breathing (4)
o Alveolar surface tension
Role of surfactant- keeps alveoli open and free of fluid and pathogens and prevents lung collapse
A lipoprotein that coats the inner surface of the alveolus and facilitates its expansion during inspiration, lowers alveolar surface tension at end-expiration, and, thereby, prevents lung collapse
What type of cells procedure surfactant?
type II alveolar cells
o Airway resistance
Airway size
Gas velocity
Normally low
Bronchodilation: decreases airway resistance
Bronchoconstriction: increases airway resistance
o Elastic recoil: Tendency of the lungs to return to the resting state after inspiration.
o Compliance: Measures lung and chest wall distensibility.
Neurochemical control of ventilation
o Central chemoreceptors reflect PACO2-stim by H+ in the CSF
Increases respiratory depth and rate
o Peripheral chemoreceptors are stimulated by hypoxemia (PAO2)
located in the aorta and carotid bodies
is responsible for all the increase in ventilation that occurs in response to arterial hypoxemia.
Bronchitis-
infection or inflammation of large airways or bronchi; self-limiting
o Caused by virus (acute)
o Usually is not bacterial and does not require antibiotics or steroids
o Accompanied a cough
Chronic c/b smoking
Hyperventilation and when does it occur?
rapid deep breathing resulting in excessive elimination of CO2.
alveolar ventilation to meet metabolic demands
o When would it occur?
Anxiety
Head Injuries
Severe Hypoxemia
Metabolic acidosis
Fever
Lung Cancer- malignant tumor growth in lung tissue (know basic facts)
o AKA: bronchogenic carcinomas
o 95% of all tumors of the lung are carcinoma.
o Survival rate is not great in 5 years
o 2nd Most frequent cause of cancer death in the US
o Heavily linked to tobacco use (small cell)
NSCLC: linked w/ squamous cell ca, adeno-, and large cell carcinoma
**note: colon ca just surpassed within last 12-18months per professor
COPD-what would an ABG look like?
chronic inflam c/b emphysema or chronic bronchitis
Respiratory acidosis due to CO2 retention with compensation
low pH
high CO2
compensated through kidney’s bicarb, if all works right
Pulmonary Embolism & V/Q mismatch
o Most s/s are silent due to the small size and the fibrinolytic system respsonse-most clots are destroyed.
o Atelectasis (complete or partial collapses of the lung or section) to the affected lung segment can occur and cause hypoxemia
o Sequelae include pulmonary edema, pulmonary HTN, shock and even death.
High mortality
o Causes a release of neurohumoral substances that cause widespread vasoconstriction all over, which pushes it to the acute state
o If you have a patient with a PE they would have a high V/Q because its impaired perfusion, nothing to do w/ vent.
Elevated D-dimer, ABG’s, CT pulm angiogram
Rotational CTA’s are replacing V/Q scans
Community Acquired PNA
o Usually follows a viral infection in upper airway
presents with an abrupt high fever, chills, shaking, and pleuritic chest pain. (in young-mid age,
more innocuous s/s in elderly)
rales/rhochi/crackles
o MC pathogen is Streptococcus Pneumoniae
Pathophysiology of Emphysema
o Emphysema is more permanent narrowing
Destruction of the alveolar walls leading to decreased lung elasticity and airflow limitation
Know definition- abnormal permanent enlargement of the lung air spaces without fibrosis, decreasing surface area available for gas exchange
MC causes are inflammation, tobacco, or environmental pollutants.
Mediator release-elastase that breakdown extracellular matrix = more inflam.
Pathophysiology of (Asthma)-true facts, pull out difference that’s linked w/ emphysema
Asthma has reverse ability
exercised induced
allergen response (IgE)
Chronic airway inflammation, bronchoconstriction, and hyperresponsiveness
Recurrent episodes of wheezing, restlessness, chest tightness, cough, bronchial edema
Exam scenario-caused by bronchial smooth muscle that causes hypertrophy and hyper reactivity as well as bronchospasm due to
chronic bronchial inflammation due to eosinophils infiltrating that area.
Pathophysiology of (TB)
TB- Mycobacterium tuberculosis infection causing granulomatous lung lesions.
Tubercle Formation
Granulomatous lesions
Airborne and droplet transmission
May remain dormant for life or cause active disease.
Caseous Necrosis- type of cell death that causes tissues to become “cheese- like.”
Chest wall disorders (kyphoscoliosis or obesity) affect on FEV1 (forced expiratory volume one second)
o Asthma and COPD decrease FEV1
airway obstruction is worse with expiration. More force or more time is required to expire a given volume of air; emptying the lungs isslowed.
o Chest wall disorders increase FEV1 (think about compliance in breathing mechanisms; lung and chest wall distensibility )
work of breathing is increased.
ventilation maybe compromised d/t decreased in tidal volume.
ARDS (acute respiratory distress syndrome)-
Clinical manifestations
severe lung injury with acute respiratory failure
o Clinical manifestations
Dyspnea and hypoxemia with poor response to oxygen supplementation
Decrease tissue perfusion, metabolic acidosis, and organ dysfunction.
Increased work of breathing, decreased tidal volume, and hypoventilation.
Hypercapnia, respiratory acidosis, and worsening hypoxemia
Respiratory failure, decreased cardiac output, hypotension, multiple organ dysfunction syndrome, and death.
ARDS (acute respiratory distress syndrome)-
Normal treatment
Mechanical ventilation with PEEP and high oxygen concentrations
Low- volume ventilation, noninvasive positive pressure ventilation, permissive hypercapnia, prone positioning, neuromuscular blockade,
extracorporeal lung assist ECMO
prophylactic immunotherapy
antibodies against endotoxins
antioxidants
surfactant replacement
Nitric oxide inhalation
inhibition of various inflammatory mediators
gene therapy
stem cells
Pulmonary Edema-
injury to capillary endothelium
if there are blockages of lymphatic vessels or heart failure, CAD, HF, can all lead to pulmonary edema.
ARDS, PE, smoke inhale, transfusion reactions, near-drowning
Pneumoconiosis-
lung disease caused by inhalation of mineral dust (coal and silica)
o Inhalation injury
Compression Atelectasis
External compression of the lung
Resorption Atelectasis (during PE)
gradual absorption of air from obstructed or hypoventilated alveoli
Transudative Effusion (heart failure or liver disease)
Watery and diffuse out of capillaries.
Exudative effusion (empyema)
less watery
high white blood cells and
plasma proteins.
Oxyhemoglobin dissociation curve – left shift results in what?
o Shift to left
Alkalosis
Hypocapnia (decrease in alveolar and blood CO2 levels
o Shifts to right
Hypercarbia (increase in carbon dioxide in the bloodstream)
Acidosis
Hyperthermia
Tension Pneumothorax (air enters but cannot exit)
o site of pleural rupture acts as a one-way valve, permitting air to enter on inspiration but preventing its escape by closing during expiration.
o Accumulation of air in the pleural space, causing lung collapse and mediastinal shift
Open pneumothorax
air pressure in the pleural space equals barometric
pressure because the air that is drawn into the pleural space during inspiration is forced back out during expiration
Pneumocytes produce what?
Are specialized cells in the alveoli of the lungs.
o Type I Pneumocytes: These thin, broad cells cover about 95% of the alveolar surface. They allow rapid gas diffusion between air and blood, facilitating gas exchange
o Type II Pneumocytes: These cells have two critical functions:
They produce surfactant, a fluid that prevents alveoli from collapsing during exhalation.
They can transform into type I pneumocytes to repair alveolar epithelium.
Cholelithiasis- formation of gallstones in the gallbladder or bile ducts
Cardinal manifestations
Epigastric and right hypochondrium pian
often referred to as biliary colic, occurs 30 mins to several hours after eating a fatty meal
Intermittent or steady and usually occurs in the RUQ, radiating to the mid upper back.
Intolerance to fatty foods
Jaundice indicates a stone is in the common bile duct.
Cholecystitis
■ Definition: Inflammation of the gallbladder, often due to gallstone obstruction.
■ Pathophysiology: A gallstone lodges in the cystic duct, causing bile stasis, inflammation, and infection.
Hepatitis C-
Viral infection affecting the liver
o Hepatitis C damages hepatocytes, leading to chronic inflammation, fibrosis, cirrhosis, and hepatocellular carcinoma.
o Responsible for most postransfusion hepatitis
o Implicated in infections related to IV drug use and HIV
o Coinfection with Hep B
o 80% of those with it develop chronic liver disease.
o No vaccine
o Give antiviral meds.
Cholecystitis-
Inflammation of the gallbladder, often due to gallstone obstruction.
o Common findings
Fever
Leukocytosis
Rebound tenderness
Abdominal muscle guarding
Serum bilirubin and alkaline phosphate levels may be elevated
Hematemesis-
vomiting of blood (usually from upper GI bleeding).
C/B: peptic ulcers, varices, diverticulosis, or malignancies
Ulcerative Colitis-
chronic inflammatory disease that causes ulceration of the colonic mucosa-
sigmoid colon and rectum.
o Presentation
Large volumes of watery diarrhea
bloody stools
cramps
urge to defecate
Can have stages of remission and exacerbation.
Primary sclerosing cholangitits (PSC) strong correlation
What type of diarrhea would you see in certain GI disorders like Pancreatic insufficiency, Crohn’s, Celiac disease?
Malabsorptive Diarrhea
Chronic diarrhea due to impaired nutrient absorption.
Can result from conditions like celiac disease, Crohn’s disease, or pancreatic insufficiency.
Hematochezia-
passage of blood from the rectum (bloody stools)
Melena-
Black, tarry stools.
About 100- 200 ml of blood in the upper GI tract, which may persist for several days after bleeding has ceased.
GIB-upper vs lower & how do you know where the bleed is coming from?
Upper GI bleeding comes from the esophagus, stomach, or duodenum.
Man: frank, bright red blood or dark, grainy digested blood (coffee grounds).
Lower GI bleeding comes from the jejunum, ileum, colon, or rectum.
Occult bleeding is caused by slow, chronic blood loss. Detectable only with positive fecal occult blood test.
What diagnosis would contribute to exudative diarrhea? (2)
o Crohn’s Disease
o Ulcerative Colitis
Malabsorptive Diarrhea
○ Definition: Chronic diarrhea due to impaired nutrient absorption.
○ Pathophysiology: Malabsorption can result from conditions like celiac disease, Crohn’s disease, or pancreatic insufficiency.
Body of the stomach (fundus) secretes what?
Hydrochloric acid and intrinsic factors
Intestinal obstruction
o Any condition that prevents the flow of chyme through the intestinal lumen or failure of normal intestinal motility in the absence of an obstructing
lesion.
o Pt presents:
Small intestine obstruction: Colicky pain caused by intestinal distention followed by N/V
Large intestine obstruction: Hypogastric pain and Abd distention.
colicky pain is NOT associated with?
pancreatitis, barrett’s esophagus, or fecal impaction.
it is asso w/ obstruction
UTI pathophysiology, risks, and pathogens (Which is false?)
o Hallmarks
Bacteriuria
Pyuria- pus in urine
Frequency
Dysuria- discomfort when urinating
o Due to retrograde movement of bacteria into the urethra, bladder, ureter, and kidney
o Inflammation of urinary epithelium caused by the bacteria usually from gut flora.
o UTI is linked to cystitis and pyelonephritis which causes more severe problems.
o Pathogen
E. Coli **
Staphylococcus saprophyticus
o What makes a patient more prone to getting UTI’s?
Sexually active
Using spermicides
Dehydrated
Living conditions, hygiene
Nephrolithiasis-
MC: calcium oxalate and calcium phosphate
kidney stones in the urinary tract
o How would the pt. present?
Renal Colic- pain
o What test would you do?
CT
MRI
Urinalysis and 24-hour urine
o What would you find on the urine analysis?
identifies calcium oxalate, calcium citrate and other significant constitutes.
Nephritic Syndrome
hematuria (usually microscopic) and red blood cell casts are present in the urine in addition to proteinuria, which is not severe;
C/B increased permeability of the glomerular filtration membrane;
contains massive amounts of protein and lipids and either a microscopic amount of blood or no blood
Acute pyelonephritis-
acute infection of the ureter, renal pelvis, and/or kidney interstitum
o High degree of renal failure if left untreated.
o One or Both kidneys are affected.
Be concerned if pt has cystitis, it can travel upstream
o Clinical manifestations:
flank/ groin pain
fever, chills
costovertebral tenderness
UTI symptoms
o WBC casts indicate pyelonephritis.
o Treat with antibiotics
Renal calculi
Kidney stones
o Most common?
Calcium oxalate and calcium phosphate: 70% to 80%
o What is it made of?
Masses of crystals, protein, or mineral salts
Portal HTN causes what other physiological conditions?
o Hepatorenal syndrome- impaired kidney function in pts with advanced liver disease.
o Splenomegaly
o Esophageal varices
GERD- acid and pepsin reflux from the stomach in to the esophagus, causing esophagitis
o Resting tone of the lower esophageal sphincter tends to be lower than normal from either transient relaxation or weakness of the sphincter.
o Junction cells at the bottom of the esophagus secrete mucin and bicarinate which help neutralize the acid contents that pass through.
o Most common outpatient complaint in the US
o Causes inflammation at the lowest esophageal sphincter site.
o Is associated with life threatening illnesses.
o Treat with proton pump inhibitors
o Where would you have metaplastic changes?
Lower esophagus
o Clinical manifestations
Heartburn from acid regurgitation, chronic cough, laryngitis, asthma attacks, sinusitis
Upper abdominal pain within 1 hour of eating
Pylori presentation-
bacterium that infects the stomach and is associated with gastric ulcers, gastritis and cancer.
o the infection damages the gastric mucosa.
Acute Gastritis (question will have a list of options that will have to do with this and figure out which is true)
Associated with:
H. pylori infection
Chronic NSAID use can lead to this and ulcerations.
Drugs
Chemicals
Metabolic disorders
o Clinical manifestations
vague Abd discomfort, epigastric tenderness, and bleeding
o Treatment:
Healing usually occurs spontaneously within a few days.
Discontinue injurious drugs.
Administer antacids.
Decrease acid secretion with a histamine type 2 (H 2 ) receptor antagonist and a proton pump inhibitor.
Duodenal ulcer
o Most common cause of peptic ulcers
o Common cause is H. pylori and overuse NSAIDs
o Clinical manifestations
Chronic intermittent pain in the epigastric area.
Pain begins 30 minutes to 2 hours after eating when the stomach is empty.
Pain is relieved by food and antacids.
Chronic PUD-causes
70% H Pylori
NSAID use
What exact part of the kidney is responsible for regulation of BP and GFR?
Juxtaglomerular cells and macula densa form the juxtaglomerular apparatus (JGA) that controls renal blood flow (RBF), glomerular filtration, and renin secretion occurs at this site.
Acute Glomerulonephritis-
inflammation of the tiny filters in the kidney
o What are some clinical manifestations as the disease progresses?
Oliguria**
Hypertension
Renal failure
Hematuria with red blood cell casts (more severe and rapidly progressive)
Primary functions of the kidney (what are all of the functions?)
A WET BED
A WET BED mnemonic:
A: Controlling acid-base balance.
W: Controlling water balance.
E: Maintaining electrolyte balance.
T: toxins and waste removal.
B: Controlling blood pressure- Renin
E: Producing the hormone erythropoietin.
D: Activating vitamin D
o Perform gluconeogenesis: Synthesis of glucose from amino acids.
o Forms urine
Neurogenic Bladder: How will the patient present?
Frequent daytime voiding: More often than every 2 hours while awake
Nocturia: Night-time voiding
Urgency: Often combined with hesitancy
Dysuria
Poor force of stream; intermittency of urinary stream
Feelings of incomplete bladder emptying, despite micturition
CKD-
progressive loss of kidney function associated with systemic diseases.
o Gradual damage to nephrons impairs infiltration, leading to fluid and electrolyte imbalances.
o Clinical manifestations do not occur until renal function declines to less than 25% of normal.
o A patient will also have HLD and DM because of vascular disease that attributes to CKD.
o Metabolic acidosis
o Hypocalcemia
o High phosphate
o Low erythropoietin
GFR-
rate at which the kidneys filter blood
o Decreased GFR indicated impaired kidney function
o Worsening filtration= low GFR
AKI and types (how will patient present-which type will it be?)
o Electrolyte abnormalities
o Metabolic Acidosis- accumulation of nitrogenous waste products in the blood
o Uremia- high level of waste products in the blood
o Increased creatinine
o Signs of fluid overload
o Oliguria- low UOP; less than 400ml per day
o Types and causes:
Prerenal: reduced blood to kidneys; MC
Hypovolemia; ex. hemorrhagic blood loss
Reduced Cardiac Output
Renal Vasomodulation/ shunting; ex. Iodine contrast, medications
Systemic Vasodilation
Intrarenal: damage to kidney tissue
MC cause: Acute tubular necrosis d/t ischemia
Postrenal: obstruction of urine flow
Bladder outlet; ex. BPH
Ureteral (bilateral obstruction)
Renal pelvis; papillary necrosis
The highest concentration of potassium is found in the cell due to the charge of that interior cell.
Keep going-You’re doing GREAT!
Crohn’s Disease-
Granulomatous colitis, ileocolitis, or regional enteritis
o Idiopathic inflammatory disorder; affects any part of the digestive tract, from the mouth to the anus.
o What is attributed to Crohn’s?
Causes “Skip” lesions
Inflamed areas mixed with uninflamed areas, noncaseating granulomas, Fistulas, deep penetrating ulcers.
Perianal disease
o Clinical Manifestations
Rectal bleeding (most common)
Diarrhea (most common)
Abdominal Tenderness
Anemia may develop d/t malabsorption of vitamin B12 and folic acid.
Bone mineral storage
○ Definition: Bone mineral storage refers to the deposition and release of minerals (such primarily calcium and phosphorus) within bone tissue.
○ Pathophysiology:
■ Deposition: Osteoblasts actively incorporate minerals into the bone matrix, especially during growth and remodeling.
■ Release: Osteoclasts resorb bone tissue, releasing stored minerals back into the bloodstream. This process is essential for maintaining blood calcium levels.
Know differences of medial and lateral epicondylitis and what attributes to
them
Medial epicondylitis - C/B damage to the muscles and tendons that control your wrist and fingers. The damage is typically related to excess or
repeated stress, especially forceful wrist and finger motions. Improper lifting, throwing, or hitting, as well as too little warmup or poor
conditioning, also can contribute to a golfer’s elbow
■S/S: Pain on the inner side of the elbow
● Stiffness/weakness when making a fist
● Weakness of the affected hand or wrist
● Numbness or tingling
○ Lateral epicondylitis - tennis elbow
Osteoblasts vs Clasts
Blasts: build bones
Clasts: break them down
Bone cellular make up
○ Definition: Bone tissue consists of specialized cells and an extracellular matrix.
○ Pathophysiology:
■ Osteoblasts: These cells synthesize and secrete the organic matrix (osteoid) of bone, which includes collagen fibers and proteoglycans. They
also regulate mineralization by promoting the deposition of calcium and phosphate crystals.
■ Osteocytes: These are mature bone cells embedded within the bone matrix. They maintain bone health by sensing mechanical stress and
regulating bone remodeling.
■ Osteoclasts: These multinucleated cells resorb bone tissue by secreting enzymes that break down the organic matrix and release stored minerals.
Age related bone loss factors
o Women- related to decreased activity, increased osteoclasts activity, changes in the osteoprotegerin, decreased levels of estrogen
o Also contributed to decreased levels of vitamin D, calcium, and magnesium
What portion of the myofibril are the parts that have contractile proteins, actin and myosin?
The sarcomere
Sarcomeres contain protein filaments (myofilaments), including thick filaments (myosin) and thin filaments (actin).
The sliding movement of these filaments during muscle contraction generates force.
Bone fracture healing phase order
o Hematoma formation occurs within hours
o Procallus formation by osteoblast osteoblasts occurs within days
o Callus formation occurs within weeks
o Replacement- Replaces the callus with lamellar bone or trabecular bone.
o Remodeling- Periosteal and endosteal surfaces are remodeled to the size and shape of the bone
before the injury.
Fracture healing part 2-Inflammatory stage
Inflammatory phase (3-4 days): Broken bones result in torn blood
vessels and the formation of a blood clot or hematoma. The
inflammatory reaction results in the release of cytokines, growth
factors, and prostaglandins, all of which are important in healing.
The fracture hematoma becomes organized and is then infiltrated by
fibrovascular tissue, which forms a matrix for bone formation and
primary callus.
Fracture healing pt 2: Reparative phase
Reparative phase (days-weeks): A thick mass of callus forms around the bone ends, from the fracture hematoma. Bone-forming cells are
recruited from several sources to form new bone, which can be seen on radiographs within 7-10 days after injury. Soft callus is organized and remodeled into hard callus over several weeks. Soft callus is
plastic and can easily deform or bend if the fracture is not
adequately supported. Hard callus is weaker than normal bone but is better able to withstand external forces and equates to the stage of “clinical union”, i.e. the fracture is not tender to palpation or with
movement.
Fracture healing pt 2:
Remodeling phase
Remodeling phase (months-years): This is the longest phase and
may last for several years. During remodeling, the healed fracture and surrounding callus respond to activity, external forces,
functional demands, and growth. Bone (external callus) which is no longer needed is removed and the fracture site is smoothed and
sculpted until it looks much more normal on an x-ray. The epiphyses
gradually realign and residual angulation may be slowly corrected, in accordance with the rules of remodeling, outlined above
Crepitus- X-ray findings
○ Definition: Crepitus is a crackling or grating sound produced when bones rub against each other or against roughened cartilage.
○ Pathophysiology:
■ Crepitus can occur due to joint degeneration (e.g., osteoarthritis), fractures, or inflammation.
Sciatica causes
o Not contributed to soft tissue abnormalities
o Found in patients with herniated discs, spinal stenosis, compression fractures,
RA presentation-What do the symptoms look like throughout the day?
symmetrical early morning stiffness that gets better throughout the day; small joints of wrists/fingers
■ Chronic inflammation leads to synovial membrane thickening, joint swelling, pain, and destruction of cartilage and bone.
■ Autoantibodies (rheumatoid factor) target synovial tissue.
OA presentation and deformities
o Worsening pain throughout the day
o Deep achy pain and stiffness in joints
o What are the nodules called in the fingers and findings when examining your patient?
■ Heberden’s nodes appear on the joint closest to the fingertip (DIP)
■ Bouchard’s nodes appear on the middle joint of the finger (PIP)
o What are you looking for at the joints?
pain, stiffness, joint enlargement, limited ROM, and deformity
NOT inflammation
Joint swelling in the fingers
Heberden’s nodes appear on the joint closest to the fingertip (DIP)
Bouchard’s nodes appear on the middle joint of the finger (PIP)
Bursitis causes
hemorrhage,
infection,
inflammation
repeated trauma
NOTHING to do w/ bone Health
Sjogren’s syndrome-How would pt present?
o Ocular oral dryness
o Autoimmunity
Immune cells attack and damage the salivary and lacrimal glands, reducing tear and saliva production.
■ This leads to dryness, discomfort, and potential complications in other organs.
Shingles (Herpes Zoster) -be able to recog picture
After a primary VZV infection (chickenpox), the virus remains dormant in sensory nerve ganglia.
Pain and paresthesia localized to a dermatome (the cutaneous area innervated by a single spinal nerve), followed by vesicular eruptions along a facial, cervical, or thoracic lumbar dermatome, then crusting
Rash does not cross body’s midline; 2 or more adjacent dermatomes can be affected
o Treatment
No cure
Antiviral to be given within first 72 hours
Tricyclic antidepressant
Seborrheic Keratosis–recog picture
benign proliferation of cutaneous basal cells that produces flat or slightly elevated lesions that may be smooth or warty in appearance
o Singular or in multiples on the chest, back, and face
o Color varies from tan to waxy yellow, flesh colored, or dark brown to black
Tx: cryotherapy w/ liquid nitro or cautery.
Malignant Melanoma-recog picture
tumor of the skin originating from melanocytes
o ABCDE rule is used to guide
Asymmetry
Border irregularity
Color variation
Diameter larger than 6 mm
Elevation that includes a raised appearance or rapid enlargement
o Most serious and most common cause of death from skin cancer
Basal Cell Carcinoma
○ Definition: Basal cell carcinoma (BCC) is the most common skin cancer, arising from basal cells in the epidermis.
○ Pathophysiology:
■ Chronic sun exposure (UV radiation) damages basal cells.
■ BCC grows slowly, rarely metastasizes, but can invade surrounding tissues.
Psoriasis
o What is it?
o Is it only related to the skin or is it systemic?
○ Definition: Psoriasis is a chronic T-cell autoimmune-mediated skin disorder characterized by thick, red, scaly plaques.silvery, elevated lesions
scalp, face, trunk, elbows or knees
relapsing, proliferative, inflammatory
○ Pathophysiology:
■ Immune system activation leads to rapid turnover of epidermal cells.
■ Abnormal keratinocyte proliferation and inflammation cause thickened skin.
epidermal turnover goes from 26-30 days down to 3-4 days; cells don’t have time to keritainze
Seborrheic keratosis (pic)
○ Definition: Seborrheic keratosis is a common benign skin tumor characterized by raised, waxy, pigmented growths.
○ Pathophysiology:
■ Exact cause is unclear, but genetic factors and sun exposure play a role.
■ Proliferation of epidermal keratinocytes leads to the formation of these lesions.
Cellulitis
o What is it and how does it present?
○ Definition: Cellulitis is a bacterial skin infection involving the dermis and subcutaneous tissues.
○ Pathophysiology:
■ Bacteria (usually Staphylococcus or Streptococcus) enter through breaks in the skin.
■ Inflammation, redness, warmth, and swelling occur.
Basic skin alteration definitions (think nevi, bulla etc.)
○ Nevi (Moles): Benign skin growths due to melanocyte proliferation.
○ Bulla: Large fluid-filled blister (>1 cm) in the epidermis or dermis.
○ Pustule: Small, pus-filled blister.
○ Erythema: Redness of the skin due to increased blood flow.
○ Lichenification: Thickening and hardening of the skin due to chronic irritation.
Wheal: elevated, irregular shaped skin edema-solid and transient
Nodule: elevated, firm, and circumscribed lesion; is deeper in the dermis than a papule; measures 1–2 cm in diameter
Tumor - elevated, solid lesion; may be clearly demarcated; is deeper in the dermis; measures greater than 2 cm in diameter
Vesicle - elevated, circumscribed, and superficial lesion; does not extend into the dermis; is filled with serous fluid; measures less than 1 cm indiameter
Basic Skin alterations-pt 2
○ Pustule - elevated, superficial lesion; is similar to a vesicle but filled with purulent fluid
○ Bulla - vesicle that measures greater than 1 cm in diameter
○ Macule - flat, circumscribed area that is a change in the color of the skin; measures less than 1 cm in diameter
○ Papule - elevated, firm, and circumscribed area; measures less than 1 cm in diameter
○ Patch - flat, nonpalpable, and irregular-shaped macule; measures more than 1 cm in diameter
○ Plaque - elevated, firm, and rough lesion with a flat top surface greater than 1 cm in diameter
○ Cyst - elevated, circumscribed, and encapsulated lesion; is in dermis or SQ layer and filled with liquid or semisolid material
○ Telangiectasia - irregular red lines; are produced by capillary dilation
Steven Johnson syndrome (1 true or false question) know definition
○ Definition: SJS is a severe, potentially life-threatening skin reaction triggered by
medications or infections.
○ Pathophysiology:
■ Immune-mediated hypersensitivity reaction leads to widespread skin detachment and mucosal involvement.
Cutibacterium acnes=acne vulgaris
○ Definition: C. acnes is a bacterium commonly found on human skin, especially in hair follicles.
○ Pathophysiology:
■ C. acnes contributes to acne vulgaris by colonizing hair follicles, leading to inflammation and comedone formation.
Dermatitis
○ Definition: Dermatitis refers to skin inflammation.
○ Pathophysiology:
■ Various causes (allergens, irritants, infections) trigger immune responses, leading to redness, itching, and rash.
Know hives (urticaria) and how it can be treated
o What type of reaction is it?
Type 1 hypersensivity reaction
pruritic area of redness w/ central pallor,
ex: wheals, welts
Tx: anti-histamines, leukotriene-receptor agonists, alpha-adrenergic agonists, and steroids
Bacterial Meningitis (organism and lab findings of CSF)
MC org: Group B-strep in infants
Strep pneumonae in adults
LP-Csf
high WBC
High protien
Low Glucose
Wound dehiscence
o How many days before it occurs after suturing?
5-12 days post-op
Referred pain vs neuropathic pain
○ Definition: Referred pain is felt in a location other than the actual site of the painful stimulus.
○ Pathophysiology:
■ Convergence of sensory nerves from different tissues leads to confusion in the brain, resulting in pain being interpreted in adjacent areas.
■ Example: Cardiac ischemia causing pain in the neck, left shoulder, and down the left arm.
Neuropathic pain is pain caused by a lesion or disease of the somatosensory nervous system. Neuropathic pain may be associated with abnormal sensations called dysesthesia or pain from normally non-painful stimuli. It may have continuous and/or episodic components. The latter resemble stabbings or electric shocks.
Tension headache
o How does patient present?
○ Definition: Tension headaches cause mild to moderate pain, often described as a tight band around the head.
■ Exact cause is unclear, but it may involve hyperexcitable peripheral afferent neurons and central pain processing abnormalities.
SubArachnoidHemorrhage- must act urgently and rule out
Uncontrolled HTN
o Thunderclap headache
o Worst HA of their lives
Swimmers ear organism- scenario on exam
o What organisms contribute to this?
Otitis Externa
Pseudomonas aeruginosa and Staphylococcus aureus.
tx: topical antibiotics: polymyxin B, neomycin, ofloxacin 5 gtts BID, or CIpro 3 gtts
Allergic reaction scenario- What are you going to do and what is the finding?
What would make it an urgent referral?
mild to severe reactions, type 1 hypersensitivity through type 4,
elevated IgE
rash/hives
ER referral for anaphylaxis or any signs of
SOA, fever, tachycardia, pallor, any GI symptoms
manage airway
epinephrin if severe
Acute Angle Glaucoma
○ Definition: Acute angle-closure glaucoma is a sudden increase in intraocular pressure due to blocked drainage of aqueous humor.
Ocular Emergency
○ Pathophysiology:
■ The iris blocks the trabecular meshwork, preventing aqueous humor drainage.
■ Rapid pressure increase leads to severe eye pain, blurred vision, and potential vision loss.
Tx: Medications.
Initial: acetazolamide, topical beta-blocker, and topical steriod
These include timolol, pilocarpine and brimonidine eye drops and oral acetazolamide.
Seizure disorder – elements to diagnose
○ Definition: Seizure disorder (epilepsy=aura) is characterized by recurrent, unprovoked seizures.
*Differentiation b/w SZ &epilepsy: LOC, Motor/Sensory deficits, and behaviors.
○ Pathophysiology:
■ Abnormal electrical activity in the brain leads to sudden, excessive neuronal firing.
■ Diagnosis involves clinical evaluation, EEG, and ruling out other causes.
Respiratory Acidosis ABG
**
Dementia
o Know basic true facts
Progressive Failure of cerebral function by
neuron degeneration, compression of brain tissue, atherosclerisis, brain trauma, genetics, CNS infections
Limiting intellectual function, memory and language
alterations in behaviors
Alz: dx only postmortem exam
hx, cog testing, brain imaging, labs.
Tx: Supportive, delay process, maintain/optimize function, and make accomodations for lost function/control
TTP
o What are the lab findings?
o Peripheral smear- a lot of RBC fragments
o increased LDH because of cell destruction
o renal dysfunction- increased BUN and creatinine
o increased or normal megakaryocytes
Know what a moderate concussion is and what is involved**
LOC >30min w/ anterograde amnesia 24 hr+
Mod GCS: 9-12;
structural injury ex: hemorrhage or contusion
Ex: basal skull fracture with no brainstem injury
Life-limiting: permanent deficits in attn, vigilance, vision/perception, language, mood/affect
Liver Failure- which hepatitis is this most associated with?
Hepatitis C
