FinalGM blueprint

Question 1

Risks for prostate cancer (What is it NOT?)

Question 2

Digital Rectal exam

Answer 2

Assessing the prostate gland. It should be
firm, not soft or enlarged.

Anatomically: posterior surface of the prostate through the rectal wall.

Question 2

Epididymitis physical exam findings and what relation to STI’s (maybe a scenario question)
What is a PREHN sign?

Answer 2

Inflammation of the epididymis (coiled tube behind testicle)
 Tenderness and swelling of epididymis.
 + Prehn sign (pain relief when the affected testicle is elevated)

Question 2

Peyronie’s disease- What is it?

Answer 2

Fibrosis and scarring of the sheath around the corpora cavernosa (erectile tissue in the penis)

o Painful bent erection that can lead to erectile dysfunction.
 Penile Pain
 Deformity
 Erectile dysfunction

Question 3

BPH symptoms (probably a question of “What is NOT a symptom?)

Answer 3

What is considered a large prostate?
 When it obstructs the urine flow significantly
o Symptoms: frequent urinating, weak stream, nocturia
o Normal size prostate: 20-25 g and 30-40 ml

Question 3

Risk factors for bacterial prostatitis (will have to answer what is not a risk factor on exam)

Answer 3

 Young middle-aged male
 Previous prostatitis
 UTIs
 Recent prostate procedures (biopsy)
 Catheter use

Question 3

Testicular cancer-basic understanding

Answer 3

 Relatively rare but highly treatable
 Is often curable, especially when detected early
 Young men (15-35 years old)

Risk factors
 Family history
 Cryptorchidism (Undescended testicles)
 Certain genetic conditions

Question 3

Priapism- What is it? (maybe a scenario question)

Answer 3

An involuntary, prolonged and painful erection that persists beyond sexual stimulation.

Question 4

Testicular torsion- Surgical emergency (What would you do for this?)

Answer 4

o Occurs with twisting of the spermatic cords and compromise blood flow.
o Sudden pain and swelling of the testicle.
o Immediate surgical detorsion to restore blood flow to the affected testicle.

Question 5

Most common cause of ADH overproduction

Answer 5

SIADH (can be caused by tumors on the pituitary)

o In SIADH, the body produces excess ADH even when the plasma osmolality is low.

Question 5

ADH role- vasopressin- is produced by the hypothalamus and released by the posterior pituitary gland.

Answer 5

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 urine back into the
bloodstream causing concentrated urine.
o Released when osmolality is increased and volume in the blood stream is decreased.

Question 6

Endocrine system specializes in secreting substances in three categories…

Answer 6

o Endocrine- affects distant cells- travel through the blood, often called hormones
o Autocrine- affects cells that produce it
o Paracrine- affects nearby cells

Question 7

Hypothyroidism

Answer 7

o Iodine deficiency is the MC cause worldwide
o Hashimoto’s disease is the most common type in the US
 Also known as Autoimmune thyroiditis
o Symptoms: fatigue, weight gain, cold intolerance, goiter

Question 7

Normal glucose and insulin homeostasis

Answer 7

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 proteolysis.

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

Question 8

Parathyroid hormone does what? (Produced by parathyroid glands)

Answer 8

 Increases serum calcium concertation by stimulating bone reabsorption.
 Enhances renal tubule reabsorption of calcium.
 Promotes activation of vitamin D, which aids in calcium reabsorption from the intestine.

Question 9

Grave’s disease presentation

Answer 9

The most common cause of hyperthyroidism
o Key features:
 It affects 7x more women than men in US
 Autoimmune disorder with antibodies targeting the thyroid-stimulating hormone receptor.
 Clinical manifestation: weight loss, palpitations, ophthalmopathy (vision changes), exophthalmos (bulging eyes), and goiter.

Question 10

Type 2 DM (True or False statements)

Answer 10

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 dysfunction.

o Common symptoms:
 Polydipsia- excessive thirst
 Polyuria- excessive urinating
 Polyphagia- excessive eating

Question 11

Polydipsia=

Answer 11

excessive thirst

Question 12

Polyphagia=?

Answer 12

Excessive eating

Question 13

Polyuria=?

Answer 13

excessive urination

Question 14

Diagnosis of DM requires what findings?**

Answer 14

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.

Question 15

Cushing syndrome (scenario)

Answer 15

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.

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

Question 15

Type 1 DM

Answer 15

o Autoimmune disorder is when pancreatic beta cells are destroyed.
o Absolute insulin deficiency.
o Requires exogenous insulin for survival

Question 15

DKA- increased glucose demands (illness or stress) and severe insulin deficiency that results in the liver producing ketones

Answer 15

o Key features: hyperglycemia, ketosis, metabolic acidosis, and dehydration

o 3 I’s that are associated
 Infection
 Ischemia
 Insulin deficiency

Question 16

Causes and complications of hyperglycemia

Answer 16

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

Question 17

Insulin resistance (skin side effect)

Answer 17

Acanthosis nigricans (dark, thickened patches) due to hyperinsulinemia.

Question 18

Anterior Pituitary produces 6 hormones

Answer 18

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

Question 19

Posterior Pituitary produces 2 hormones

Answer 19

o Oxytocin- causes uterine contractions and milk ejection in lactating women
o ADH

Question 20

SIADH causes what type of hyponatremia?

Answer 20

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

Question 21

Venous Insufficiency- How will the patient present?

Answer 21

 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.

Question 22

HTN Emergency- vs urgency

Answer 22

severe high blood pressure leading to end- organ damage with systolic BP >180 and diastolic BP > 120

o With urgency there are not exacerbated signs and symptoms
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

Question 22

STEMI- complete occlusion of the coronary arteries leading to myocardial ischemia and necrosis.

Answer 22

EKG- ST elevation in specific leads

$$what leads??

Question 23

Risk factors for DVT

Answer 23

o Immobility
o Surgery

o Virchow’s Traid
 Hypercoagulability of blood
 Impaired venous blood flow (stasis)
 Vessel injury/ endothelial damage

Question 23

AMI & Location of MI diagnostic test

Answer 23

o Results from coronary artery occlusion
o ECG- shows the location of damage (anterior, inferior or lateral)
o Troponin level and EKG findings guide diagnosis

Question 24

ACS presentation

Answer 24

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

Question 25

CAD presentation

Answer 25

Angina: chest pain or discomfort due to reduced blood flow to the heart.

Question 25

Venous stasis ulcers are due to what?

Answer 25

Impaired blood return, leading to tissue
hypoxia and skin breakdown. Compression therapy and wound care for treatment

Question 26

NSTEMI versus Unstable Angina is determined by what test?

Answer 26

Troponin elevation is seen in NSTEMI

Question 27

Purkinje fibers-

Answer 27

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

Question 28

AAA (abdominal aortic aneurysm)

Answer 28

o Pathological dilation of the abdominal aorta

o Will present with:
 Abd pain, often radiating to the back
 Hypertension
 Pulsatile abdominal mass *** (dead give away)

Question 29

Raynaud’s phenomenon-

Answer 29

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

Question 30

Cardiogenic shock signs of inadequate tissue perfusion

Answer 30

o Oliguria***- reduces urine output due to poor organ perfusion
o Hypotension
o Cool extremities
o Altered mental status

Question 31

HF presentation and diagnostics- due to impaired cardiac function (scenario question).

Answer 31

Presentation is dyspnea (shortness of breath), fluid retention and fatigue.
o Laboratory- BNP levels (B- type natriuretic peptide)
The most appropriate diagnostic test- Echocardiogram

Question 32

Blood flow pattern through the valves of the heart (just 1 question)

Answer 32

o Right atrium → tricuspid valve → right ventricle → pulmonary valve →pulmonary artery → lungs

o Left atrium → mitral valve → left ventricle → aortic valve → aorta → systemic circulation

Question 33

The anterior wall of the heart is oxygenated by which coronary artery?

Answer 33

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

Question 34

Myocardium oxygen extraction

Answer 34

o Extracts oxygen from coronary blood flow during diastole to meet metabolic demands.
o Reduced oxygen supply can lead to ischemia

Question 35

What is the most common cause of an MI?

Answer 35

o Coronary atherosclerosis (scenario question)
o Women present differently- how will she present?
o Clinical manifestations:
 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

Question 36

Mechanisms of breathing (4)

Answer 36

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.

Question 37

Neurochemical control of ventilation

Answer 37

o Central chemoreceptors reflect PACO2
 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.

Question 38

Bronchitis-

Answer 38

infection or inflammation of large airways or bronchi; self-limiting

o Caused by virus
o Usually is not bacterial and does not require antibiotics.
o Accompanied a cough

Question 39

Hyperventilation and when does it occur?

Answer 39

rapid deep breathing resulting in excessive elimination of CO2.

o When would it occur?
 Anxiety
 Head Injuries
 Severe Hypoxemia
 Metabolic acidosis
 Fever

Question 40

Lung Cancer- malignant tumor growth in lung tissue (know basic facts)

Answer 40

o Also known as bronchogenic carcinomas
o 5% of all tumors of the lung are carcinoma.
o Survival rate is not great in 5 years
o Most frequent cause of cancer death in the US
o Heavily linked to tobacco use

**note: colon ca just surpassed within last 12-18months per professor

Question 41

COPD-what would an ABG look like?

Answer 41

 Respiratory acidosis due to CO2 retention with compensation
low pH
high CO2?
compensated through kidney’s bicarb

Question 42

Pulmonary Embolism & V/Q mismatch

Answer 42

o Most s/s are silent due to the fibrinolytic system
destroying most of the Pes.
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.
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 and ventilation due to the obstruction of the thrombus

Question 43

Community Acquired PNA

Answer 43

o Usually follows a viral infection.
The Pt usually presents with an abrupt high fever, chills, shaking, and pleuritic chest pain. (in young-mid age, more innocuous s/s in elderly)
o MC pathogen is Streptococcus Pneumoniae

Question 44

Pathophysiology of Emphysema

Answer 44

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

 MC causes are inflammation, tobacco, or environmental pollutants.

Question 45

Pathophysiology of Emphysema, (Asthma) and TB

Answer 45

Asthma has reverse ability

 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.

Question 45

Pathophysiology of Emphysema, Asthma and (TB)

Answer 45

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.”

Question 46

Chest wall disorders (kyphoscoliosis or obesity) affect on FEV1 (forced expiratory volume one second)

Answer 46

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 is
slowed.

o Chest wall disorders increase FEV1 (think about compliance in breathing mechanisms; lung and chest wall distensibility )
 work if breathing is increased.
 ventilation maybe compromised d/t decreased in tidal volume.

Question 47

ARDS (acute respiratory distress syndrome)-
Clinical manifestations

Answer 47

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.

Question 48

ARDS (acute respiratory distress syndrome)-
Normal treatment

Answer 48

 Mechanical ventilation with PEEP and high oxygen concentrations
 Low- volume ventilation, noninvasive positive pressure ventilation, permissive hypercapnia, prone positioning, neuromuscular blockade,
extracorporeal lung assist
 prophylactic immunotherapy
 antibodies against endotoxins
 antioxidants
 surfactant replacement
 Nitric oxide inhalation
 inhibition of various inflammatory mediators
 gene therapy
 stem cells

Question 49

Pulmonary Edema-

Answer 49

injury to capillary endothelium

Question 50

Pneumoconiosis-

Answer 50

lung disease caused by inhalation of mineral dust (coal and silica)

o Inhalation injury

Question 51

Compression Atelectasis

Answer 51

External compression of the lung

Question 52

Resorption Atelectasis (during PE)

Answer 52

gradual absorption of air from obstructed or hypoventilated alveoli

Question 53

Transudative Effusion (heart failure or liver disease)

Answer 53

Watery and diffuse out of capillaries.

Question 54

Exudative effusion (empyema)

Answer 54

less watery
high white blood cells and
plasma proteins.

Question 55

Oxyhemoglobin dissociation curve – left shift results in what?

Answer 55

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

Question 55

Tension Pneumothorax (air enters but cannot exit)

Answer 55

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

Question 56

Open Pneumothorax

Answer 56

air pressure in the pleural space equals barometric pressure because air that is drawn into the pleural space during inspiration is forced back out during expiration.
Usually, it happens during open chest wounds or physical defects caused by trauma.

Question 57

Pneumocytes produce what?

Answer 57

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.

Question 58

Cholelithiasis- formation of gallstones in the gallbladder or bile ducts

Answer 58

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 right upper quadrant, radiating to the mid upper back.

 Intolerance to fatty foods
 Jaundice indicates a stone is in the common bile duct.

Question 59

Hepatitis C-

Answer 59

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.

Question 59

Cholecystitis-

Answer 59

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

Question 60

Hematemesis-

Answer 60

vomiting of blood (usually from upper GI bleeding).

C/B: peptic ulcers, varices, diverticulosis, or malignancies

Question 60

Ulcerative Colitis-

Answer 60

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.

Question 61

What type of diarrhea would you see in certain GI disorders like Pancreatic insufficiency, Crohn’s, Celiac disease?

Answer 61

Malabsorptive Diarrhea
 Chronic diarrhea due to impaired nutrient absorption.
 Can result from conditions like celiac disease, Crohn’s disease, or pancreatic insufficiency.

Question 61

Hematochezia-

Answer 61

passage of blood from the rectum (bloody stools)

Question 62

Melena-

Answer 62

Black, tarry stools.
About 100- 200 ml of blood in the upper GI tract, which may persist for several days after bleeding has ceased.

Question 63

GIB-upper vs lower & how do you know where the bleed is coming from?

Answer 63

 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.

Question 64

What diagnosis would contribute to exudative diarrhea? (2)

Answer 64

o Crohn’s Disease
o Ulcerative Colitis

Question 65

Body of the stomach (fundus) secretes what?

Answer 65

Hydrochloric acid and intrinsic factors

Question 65

Intestinal obstruction

Answer 65

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.

Question 66

UTI pathophysiology, risks, and pathogens (Which is false?)

Answer 66

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

Question 67

Nephrolithiasis-

Answer 67

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.

Question 68

Acute pyelonephritis-

Answer 68

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.

o Clinical manifestations:
 flank/ groin pain
 fever, chills
 costovertebral tenderness
 UTI symptoms

o WBC casts indicate pyelonephritis.
o Treat with antibiotics

Question 69

Renal calculi

Answer 69

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

Question 70

Portal HTN causes what other physiological conditions?

Answer 70

o Hepatorenal syndrome- impaired kidney function in pts with advanced liver disease.
o Splenomegaly
o Esophageal varices

Question 71

GERD- acid and pepsin reflux from the stomach in to the esophagus, causing esophagitis

Answer 71

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

Question 72

Pylori presentation-

Answer 72

bacterium that infects the stomach and is associated with gastric ulcers and cancer.
o the infection damages the gastric mucosa.

Question 73

Acute Gastritis (question will have a list of options that will have to do with this and figure out which is true)

Answer 73

 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.

Question 74

Duodenal ulcer

Answer 74

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.

Question 75

What exact part of the kidney is responsible for regulation of BP and GFR?

Answer 75

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.

Question 75

Acute Glomerulonephritis-

Answer 75

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)
 Proteinuria exceeding 3-5 g/day with albumin (more severe and rapidly progressive)

Question 76

Primary functions of the kidney (what are all of the functions?)
A WET BED

Answer 76

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

Question 77

Neurogenic Bladder: How will the patient present?

Answer 77

 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

Question 78

CKD-

Answer 78

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 hyperlipidemia because of vascular disease that attributes to CKD.
o Metabolic acidosis
o Hypocalcemia
o High phosphate
o Low erythropoietin

Question 79

GFR-

Answer 79

rate at which the kidneys filter blood

o Decreased GFR indicated impaired kidney function
o Worsening filtration= low GFR

Question 80

AKI and types (how will patient present)

Answer 80

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

Question 81

Cystitis-What are you worried about in a patient with Cystitis?

Answer 81

 Pyelonephritis
 What would the step of symptoms that would make you concerned?

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Question 81

Nephritic syndrome-

Answer 81

C/B increase permeability of the glomerular
filtration membrane.
Exam findings:
 Hematuria and red blood cell casts are present in the urine.
 Proteinuria is present but is usually not as severe

Question 82

The highest concentration of potassium is found in the cell due to the charge of that interior cell.

Answer 82

Keep going-You’re doing GREAT!

Question 83

Crohn’s Disease-

Answer 83

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.

Question 84

Bone mineral storage

Answer 84

○ 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.

Question 85

Know differences of medial and lateral epicondylitis and what attributes to
them

Answer 85

Know differences of medial and lateral epicondylitis and what attributes to
them

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Question 86

Bone cellular make up

Answer 86

○ 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.

Question 87

Age related bone loss factors

Answer 87

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

Question 87

Basic Bone structures
o What are the types of cells that are responsible and that determine the increase and decrease of stable bone health in pts?

Answer 87

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Question 88

What portion of the myofibril are the parts that have contractile proteins, actin and myosin?

Answer 88

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.

Question 89

Bone fracture healing phase order

Answer 89

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.

Question 90

Crepitus- X-ray findings

Answer 90

○ 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.

Question 91

Sciatica causes

Answer 91

o Not contributed to soft tissue abnormalities
o Found in patients with herniated discs, spinal stenosis, compression fractures, Piriformis Syndrome:

Question 92

RA presentation-What do the symptoms look like throughout the day?

Answer 92

symmetrical early morning stiffness that gets better throughout the day

■ Chronic inflammation leads to synovial membrane thickening, joint swelling, pain, and destruction of cartilage and bone.
■ Autoantibodies (rheumatoid factor) target synovial tissue.

Question 93

OA presentation and deformities

Answer 93

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?

o What are you looking for at the joints?

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Question 94

Bursitis causes

Answer 94

hemorrhage,
infection,
inflammation

Question 95

Sjogren’s syndrome-How would pt present?

Answer 95

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.

Question 96

Shingles (Herpes Zoster) -be able to recog picture

Answer 96

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

Question 97

Seborrheic Keratosis–recog picture

Answer 97

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

Question 98

Malignant Melanoma-recog picture

Answer 98

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

Question 98

Basal Cell Carcinoma

Answer 98

○ 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.

Question 99

Psoriasis
o What is it?
o Is it only related to the skin or is it systemic?

Answer 99

○ Definition: Psoriasis is a chronic autoimmune skin disorder characterized by red, scaly plaques.
○ Pathophysiology:
■ Immune system activation leads to rapid turnover of epidermal cells.
■ Abnormal keratinocyte proliferation and inflammation cause thickened skin.

Question 100

Seborrheic keratosis (pic)

Answer 100

○ 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.

Question 101

Cellulitis
o What is it and how does it present?

Answer 101

○ 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.

Question 102

Basic skin alteration definitions (think nevi, bulla etc.)

Answer 102

○ 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.

Question 103

Steven Johnson syndrome (1 true or false question) know definition

Answer 103

○ 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.

Question 104

Cutibacterium acnes

Answer 104

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Question 105

What organism is responsible for acne vulgaris?
o What does it look like on the patient?

Answer 105

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Question 106

Dermatitis

Answer 106

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Question 107

Know hives (urticaria) and how it can be treated
o What type of reaction is it?

Answer 107

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Question 108

Bacterial Meningitis (organism and lab findings of CSF)

Answer 108

MC org: **
high WBC
High protien
Low Glucose

Question 109

Wound dehiscence
o How many days before it occurs after suturing?

Answer 109

5-12 days post-op

Question 110

Referred pain vs neuropathic pain

Answer 110

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Question 111

Tension headache
o How does patient present?

Answer 111

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Question 112

SAH- must act urgently and rule out

Answer 112

Uncontrolled HTN
o Thunderclap headache
o Worst HA of their lives

Question 113

Swimmers ear organism- scenario on exam
o What organisms contribute to this?

Answer 113

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Question 114

Allergic reaction scenario- What are you going to do and what is the finding?
What would make it an urgent referral?

Answer 114

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Question 115

Acute Angle Glaucoma

Answer 115

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Question 116

Seizure disorder – elements to diagnose

Answer 116

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Question 117

Respiratory Acidosis ABG

Answer 117

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Question 118

 Dementia
o Know basic true facts

Answer 118

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Question 119

TTP
o What are the lab findings?

Answer 119

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

Question 120

Ocular emergency! What could it be and what are you going to do with that patient?

Answer 120

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Question 121

Know what a moderate concussion is and what is involved**

Answer 121

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Question 122

Liver Failure- which hepatitis is this most associated with?

Answer 122

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