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.
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.
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
