PATHO FINAL

Question 1

S/s of upper brain lesions

Answer 1

Upper:
Located in the brain + down the spinal cord. They send info down a descending tract.

S/S:
-weakness + loss of voluntary motion
-spinal reflexes remain intact but cannot be regulated by the brain.
-increased muscle tone,
hyperreflexia, spasticity

Question 2

S/S Lower brain lesions

Answer 2

Lower:
send axons out of the spinal cord and innervating the target tissue.

S/S:
-affects neurons directly innervating muscles
-irritated neurons (spontaneous muscle contractions/fasciculations)
-Death of neurons; spinal reflex lost, flaccid paralysis, denervation atrophy of muscles

Question 3

What is muscular dystrophy? 2 kinds?

Answer 3

A number of genetic disorders that are progressive + degenerative and involve necrosis of skeletal muscle.
-Duchenne MD, Becker MD

Both have a defective protein (dystrophin), lack dystrophin and are sex-linked disorders.

-The contractile proteins (actin/myosin) do not effectively contract
-disuse atrophy.
-As muscle cells die, they get replaced with fat. → pseudohypertrophy

Duchenne’s vs Beckers
Duchenne’s: None or very little dystrophin. Most common. more severe affect in dystrophin and is rapidly progressing.

Beckers: Diminished/ low amounts of dystrophin. normally s/s between 3-5 yo and slower progression

Question 4

S/S of muscular dystrophy

Answer 4

DMD: appear at age 2-3 w/ motor weakness and regression becomes apparent.

BMD: appears during childhood/adolescence

-initial weakness in legs/pelvic girdle, walk w/ waddle, difficulty climbing steps
-Gower maneuver

-as it progresses, weakness spreads to other muscles like respiratory and cardiac -> cardiac myopathy (weakening of heart muscle)

Question 5

Understand the pathophysiology, etiology, s/s, treatments (if any) for myasthenia gravis

Answer 5

It is an autoimmune disorder where Ach receptors in the neuromuscular junction are destroyed by the immune system. Weakness develops from proximal-distal. When severely advanced, pt undergoes myasthenia crisis- respiration is affected; skeletal muscles also lose Ach receptors.

etiology
-idiopathic (cause not fully known)
-mostly seen in women younger than 40, over 50 for men

S/S
-Most commonly affected muscles
-facial and ocular muscles -> ptosis, diplopia (double vision)
-arms and legs
-muscle weakness in face, eyes, arms, legs,
impaired vision/speech, loss of spontaneous facial expressions, face appears to droop b/c the muscles cannot contract.

Treatment
-Tensilon test- admin Ach inhibitor and seeing if there is an improvement in skeletal muscle function.
give something to inhibit acetylcholinesterase, the Ach will stay longer at the nmj, increased probability of finding a receptor, increasing muscle activity

-anticholesterolemic drugs
-immunosuppressive drugs
-thymectomy (remove thymus)
-plasmapheresis - allows you to remove antibody attacking receptors

Question 6

Understand the pathophysiology, etiology, s/s, treatments (if any) for multiple sclerosis

Answer 6

An autoimmune disease with progressive demyelination of neurons in brain + spinal cord (CNS). The immune system attacks the myelin sheath. Demyelinated/sclerotic patches develop through white matter of the CNS.

Variation in effects and progression, 2ppl can have MS w/ different S/S due to different parts of brain becoming sclerotic.

-affects sensory + motor neurons
-intellectual function is not affected

-pt has periods of remission and exacerbation. clinician goal is to extend remission, shorten exacerbation

etiology
-onset 20-40, more common in woman
-cause = unknown, but thought to be autoimmune
-some genetic, immunologic, and environmental components; multifactorial

s/s
-determined by areas that are demyelinated
first effects: blurred vision, weakness in legs, diplopia
-numbness, burning, tingling in certain areas, sensory fibers damaged causing neuropathy
-ulcers related to immobility
-bladder dysfunction
-abnormal gait

Treatment
-modify the course, progression, and symptoms of disease, treat symptoms

-corticosteroids/glucocorticoids to control acute attacks, decrease inflammation, suppress IS,

beta interferon; Shortens exacerbations, lengthen remission.

-

Question 7

Clinically Isolated Syndrome (MS)

Answer 7

first episode of neurologic symptoms caused by inflammation and demyelination of the CNS. The first episode must last 24hrs. The clinician feels the episode is related to MS but nothing happens after that episode.

Question 8

Relapsing-remitting MS

Answer 8

-MOST COMMON MS
clearly defined attacks of new or increasing neurologic symptoms. Acute worsening w/partial or complete recovery and stable between relapses.

-characterized by exacerbations and remissions. You have exacerbations, s/s appear for a while, then you go into remission, regain lost function, the more times you get exacerbations, during remission you won’t go back to normal function.

Question 9

Primary progressive MS

Answer 9

Continuous neurologic deterioration from the onset of symptoms w/out relapse and remission.

-exacerbations and small remissions, but it is a progressive loss of function.

Question 10

Secondary progressive MS

Answer 10

follows an initial relapsing-remising course.
-combo of RR + PP MS

Most ppl are diagnosed w/ RRMS will eventually transition to secondary progressive

Question 11

Understand the different types or nerve injuries and whether or not the nerve can recover
from the injury

Answer 11

Peripheral nerve injuries
-demyelination: schwann cell disorder, damage to myelin sheath
-axonal degeneration: not properly relaying APs.
-damage to LMN cell bodies in the spinal cord
-damage to axons in the spinal/peripheral nerves
-nerve cannot recover

Mononeuropathies - a single nerve is affected/damaged
ex: carpal tunnel syndrome
caused by local trauma/injury, repetitive use, broken bone, tourniquet on too long, infection
-nerve can recover

Treat: NSAIDS, immobilization

Polyneuropathies - damage to multiple nerves, more common.
-Demyelination or axonal degeneration
-if ANS involved-, lose autonomic function > ortho hypotn, constipation, impotence (inability to maintain erection)
-nerve cannot recover

-can result from immune mechanisms (Ex: Guillain Barre syndrome), or toxic agents like arsenic, lead, alcohol.

Question 12

Understand the pathophysiology, etiology, s/s and treatment (if any) for Parkinson’s
disease

Answer 12

Parkinson’s: damage to basal nucleus/ganglia. The basal ganglia inhibit and regulate movement patterns.
-progressive degenerative changes in basal nucleus
-diminished amounts of dopamine (ensure smooth movement)
-imbalance between excitatory and inhibitory signals in the basal nucleus- excess stimulation. Muscles get too active without enough control.

S/S
-fatigue
-muscle weakness
-loss of spontaneous facial expressions
-tremors in hands @ rest
-postural instability
-if pt also has degeneration of cortical neurons-> dementia
-bradykinesia (slow movement)

Treatment:
-dopamine replacement therapy; but since dopamine can’t cross the blood-brain, can admin L-Dopa, a precursor to dopamine, because it can cross blood-brain barrier, & can be converted to dopamine, improving mobility in some individuals.
-give drugs that block the breakdown of L-Dopa

Question 13

True or false, everyone who has tremors has Parkinson’s

Answer 13

false

Question 14

Understand the pathophysiology, etiology, s/s and treatment (if any) for ALS and s/s
associated with the disorder

Answer 14

ALS is damage to upper + lower motor neurons.
-survival 2-5 years from onset.
-UMN Damage: weakness, lack of motor control + spinal reflexes, stiffness, spasticity, hyperreflexia

-LMN Damage: irritation -> fasciculations
-decreased neuron firing causing weakness, denervation atrophy, hyporeflexia

S/S
-muscle cramping
-weakness
-muscle atrophy
-impaired chewing, swallowing, speech

Treat:
riluzole, but only extends life 2-3m w/out relieving symptoms

-Edavarone - decreases decline of physical function of ALS by 33%

Question 15

Know the difference between vasogenic and cytogenic cerebral edema

Answer 15

Vasogenic Edema: accum. extracellular fluid
Extracellular fluid builds up in the brain because of impaired blood-brain barrier function. This leads to the transfer of water and proteins from the blood vessels (vascular space) into the interstitial space around the brain cells.

the patient might be going in and out of consciousness. It usually happens in things like hemorrhages, brain injuries, or infections like meningitis.

Cytotoxic edema: accum of intracellular fluid
caused by a low salt level in the blood, like water intoxication or severe hyponatremia.

If prolonged, cells will rupture, damaging surrounding cells. Person will go into stupor/coma.

Question 16

Know the different types of hydrocephalus and treatments

Answer 16

Noncommunicating/Obstructive hydrocephalus:
obstruction of CSF flow, pressure behind obstruction builds up

Communicating hydrocephalus:
malabsorption of CSF, making more CSF than absorbing.
-In children, babies head enlarge bc fontanels have not fused
-adults and older children, ICP ↑ bc skull can’t expand.

Treatments:
-Remove obstruction (obstructive hydrocephalus)

-Provide a shunt for CSF, This will get drainage of CSF from ventricles in brain where excess CSF is made, and it will go into cavity and will get reabsorbed by the body. Shunts could get infected/ blocked.

Question 17

Know the causes and difference between primary and secondary brain injury

Answer 17

Primary injuries: Initial insult done to brain. Immediate response to initial injury.
-focal lesions like contusions(bruising on surface of brain), hemorrhage (bleeding)
-diffuse injuries; widespread injury like concussion, diffuse axonal injury

2ndary injury:
brain swelling, infection, ischemia
-more damage than primary

Question 18

What are the different types of hematoma as it relates to where the blood is located

Answer 18

Epidural hematoma- collection of blood above Dura mater, between the skull

Subdural hematoma- accum. of blood between Dura mater + Arachnoid mater

Subarachnoid hemorrhage - bleeding into subarachnoid space

Intracerebral hematoma - bleeding in the brain tissue itself

Question 19

What is the difference between a concussion and a contusion and what are some s/s of
each

Answer 19

A contusion is bruising on the surface of the brain. It is caused by direct force, depressed skull fracture, or closed acceleration-deceleration injury. (brain hits the skull during fast movement, like a car accident).

-s/s depend on size + amount of cerebral edema, main goal is to prevent secondary injury

A concussion is a temporary/transient neurological impairment caused by mechanical force to the brain and can lead to loss of consciousness, usually recovers within 24hrs.
-post concussion syndrome-> headache, irritability, insomnia, poor concentration, amnesia
-chronic concussion leads to chronic traumatic encephalopathy (perm damage to brain)
-test to see reaction time, attention span, memory and repeat if it decreased

The difference between contusion/concussion is that in concussions they will lose consciousness.

Question 20

What is the difference between a TIA and a CVA, what are some causes and possible treatments (if any) for each

Answer 20

Transient Ischemic Attacks (TIA)

-‘brain angina’
-temporary reduction of blood flow to brain, after a few minutes reestablished & no loss of function. Results in focal ischemia.

Causes: partial occlusion of an artery due to atherosclerosis, small embolus, or vasospasm.

The more frequent the TIAS & the longer the duration, indicator that within the next 3 months pt will have a full blown CVA
Treat: warfarin - blood thinner

Cerebrovascular Accident (CVA)/ stroke
Total occlusion by a clot; either thrombus or embolus.
-Infarct in brain-> tissue necrosis
-ruptured vessel -> hemorrhagic stoke

causes: diabetes, htn, elevated cholesterol, hyperlipidemia, atherosclerosis, history of TIAS

Treat: preserve brain tissue, 2ndart stroke prevention, minimize long term disability
-depends on cause
-clot buster (TPA) only if you ruled out hemorrhagic stroke
-surgery (hemorrhagic stroke)

Question 21

What are the differences between tonic-clonic seizure, atonic seizure, myotonic seizure,
focal seizure with impairment of consciousness and unimpaired consciousness?

Answer 21

Tonic-clonic seizure: Body stiffens followed by rhythmic muscle contraction, loss of consciousness. Tonic + clonic seizure.

Atonic seizure: loss of muscle tone

Myotonic/myoclonic seizure: Voluntary muscles of legs and arms contract, body stiffens, legs and arms extend.

Focal seizures: unprovoked seizure
WITHOUT IMPAIRMENT OF CONSC./AWARENESS
-abnormal electric activity, limited to one hemisphere.
-may be preceded by an aura (sign seizure is coming)
-don’t lose consciousness
-clinical s/s depend on area of brain affected

WITH IMPAIRMENT OF CONSC./AWARENESS
-abnormal discharge moves from 1 hemisphere to other
-accompanied by repetitive activity (lip smacking, patting/ rubbing clothes)
-confusion during postictal period (after seizure)
-hallucinations

Question 22

What are the different types of dementia?

Answer 22

dementias are caused by permanent damage to the brain, as it progresses more + more areas are affected.

Alzheimer’s: amyloid plaques/neuritic plaques deposited in the brain, brain atrophy, microtubules & microfilaments become tangled. Tau protein is supposed to help keep structures stable, but in Alzheimer’s it becomes abnormal and causes tangles. Can no longer transmit info along axon ->depolymerization.
-decreased ACH and begins with memory issues.
-personality changes as it progresses

Vascular dementia: caused by cerebrovascular disease- causing small brain infarctions (mini strokes), w/ischemic parts in the brain that die.

Frontotemporal dementia: atrophy of frontal + temporal lobes of the brain -> presents w/disruptive behavior
-behavior/language changes
-disruptive behavior, impulsive acts/apathy

Question 23

what are the different stages of Alzheimer disease?

Answer 23

Initial: short term memory loss (2-4years)

Moderate: complete global cognitive impairment (2-10yrs)
-lose language skills, spatial relationships, problem solving, depression, confusion, disorientation, lack of insight, inability to carry on daily activities

Severe: loss of ability to respond to environment; require total care, bedridden (1-3+yrs) to live

Question 24

What is the difference between focal and global ischemia, what are common cause of each?

Answer 24

Focal ischemia: cerebral artery occlusion, leads to a stroke.

Global cerebral ischemia: loss of blood flow/perfusion to the entire brain due to a secondary event (MI, severe shock). Happens during severe shock or cardiac arrest. The brain cannot meet the metabolic demands of the whole brain.

mild cases of ischemia may cause confusion, neurological dysfunction -> temporary symptoms w/full recovery, no permanent damage

-severe prolonged ischemia: necrosis of infarction + can result in coma and vegetative state/death. Brain cells die

Question 25

Know the types of brain tumors, which one is the most common types, which one is most aggressive?

Answer 25

primary intracranial tumors of neuroepithelial tissue -astrocytoma most common type -glioblastoma multiforme: most aggressive type Focal disturbances - where tumor is/growing dysfunction of particular brain areas, seizures, hallucinations, weakness, palsies in specific areas, sensory deficits Generalized disturbances - anything related to increased ICP -headache, vomit, visual problems

Question 26

Why can 2 people who are suffering from a TIA present with very different s/s?

Answer 26

S/S varies depending on location of ischemia

Question 27

What is the pathophysiology, s/s, etiology of vaginitis and cervicitis; how would you tell the difference between the two?

Answer 27

Vaginitis: inflammation of the vagina -thin, white, burning, grey discharge -itching -redness -swelling [Bacterial vaginitis] milky discharge, potent fishy odor Cervicitis: inflammation of the cervix Acute/chronic -primary infection of the cervix -secondary infection from the vagina or uterus [Acute] -redness, edema, mucopurulent discharge [Chronic] ulcerated or normal in appearance, cysts

Question 28

s/s of endometrial cancer in postmenopausal women

Answer 28

-majority of cases 55-65 y.o -bleeding after menopause or bleeding in between periods or excessive prolonged bleeding. -sometimes caused by administering estrogen w/out progesterone.

Question 29

What is the main cause of cervical cancer?

Answer 29

Main cause is HPV. -First women will display dysplasia (pre-cancerous state), determined by pap smear and look at cells. Majority of cervical dysplasia resolves on it's own. What determines whether HPV / dysplasia resolve itself depends how deep the infection goes into the cervix, seen by biopsy.

Question 30

What is meant by retocele, cystocele and uterine prolapse; what are the different degrees of prolapse?

Answer 30

Rectocele: herniation of rectum into vagina Cystocele: herniation of bladder into vagina Uterine prolapse: [1st degree] uterus enters vagina [2nd degree] uterus drops through the vagina [3rd degree] cervix is outside vagina

Question 31

What is Candidiasis and what predisposes a woman to developing this type of infection?

Answer 31

Yeast infection caused by Candida albicans, seen in women following antibiotic treatment- the good bacterium in vagina prevents proliferation of bad bacteria + yeast spores. Antibiotics will decrease good bacteria, making them prone to yeast infections. -triggered by immune-deficiency states + increased glucose levels

Question 32

What is polycystic ovary syndromes, what are some s/s?

Answer 32

Characterized by chronic anovulation - women does not ovulate. -amenorrhea (no menstrual cycle) or irregular menses. -LH > FSH, stimulating androgen production which interferes w/ovulation. -ovaries have many Un ovulated follicles -acne, hirsutism -hyperinsulinemia -> insulin resistance -weight gain

Question 33

What is the difference between PMS and PMDD?

Answer 33

PMS: -breast swelling/tenderness -bloating/water retention -changes in bowel habits -sleep pattern changes, fatigue, lack of energy -decreased sexual desire, pain, headaches, migraines, aching muscles/joints, lower back pain prior to menstrual bleeding, aggression, withdrawal from family + friends -symptoms released once menses starts -treated w/ diuretics, NSAIDS, oral contraceptives, change lifestyle PMDD: -Breast tenderness, weight gain, abdominal distention/bloating, irritability, emotional labile, headache, depression -> extreme mood shifts -need 5 or more symptoms w/ 1 related to mood -symptoms interfere w/ activities, work, school, relationships -extreme feelings of depression treatment: low dose fluoxetine/prozac an SSRI

Question 34

What is endometriosis and what are some suggestive causes of it; how can it be treated?

Answer 34

Endometrial tissue is located outside of the uterus/ endometrium. Theories of causes Retrograde menstruation - during flow phase, some tissue comes out vagina and goes up into uterine tubes + abdominal cavity. Metastasis through lymphatics/vascular system - cells metastasize through lymphatic and circulation system. Activation of dormant cells that were always there TREATMENT -remove the offending tissue, pain management w/aspirin, NSAIDS, and acetaminophen. -stop menstrual periods w/progestin to allow the endometrial tissue to regress, then try to have a child, low dose birth control, GnRH antagonists that decrease LH & FSH

Question 35

What are women who suffer from endometriosis in such pain around/during their periods?

Answer 35

Ectopic implants respond to hormones. They go through the same changes that endometrium goes through during menstrual cycle. During flow phase, ectopic endometrial tissue has nowhere to go. Local areas of inflammation as ectopic tissue undergoes apoptosis. Tissue bleeds + dies., has nowhere to go. Pain and adhesions result from scar tissue.

Question 36

What is some s/s of ovarian cancer and which women are at high risk for developing ovarian cancer?

Answer 36

ovulatory age most significant risk factor BRCA1/BRCA2 increase susceptibility (tumor suppressor genes) -high fat diet + genital talc powders linked S/S vague GI symptoms -feeling bloated, full, indigestion, backache, sudden wt. gain

Question 37

What is meant by dysmenorrhea, amenorrhea, menorrhagia?

Answer 37

Dysmenorrhea - pain or discomfort w/menstruation Amenorrhea - absence of menstruation/no period [primary] fail to menstruate by age 13-15 if it is accompanied by failure of developing secondary sexual characteristics -> gonad dysfunction [2ndary] no menstruation for 6months in a women who has a regular cycle; pituitary tumors, anorexia, strenuous physical exercise (athlete) Menorrhagia - excessive menstruation

Question 38

What are some treatments for breast cancer, how do the treatments work?

Answer 38

-hormonal manipulation used to block effects of estrogen receptors on breast cancer: estrogen, HER-2, progesterone Herceptin- blocks HER-2 receptor Tamoxifen - blocks estrogen receptor -triple negative breast cancer if no estrogen, HER 2, or progesterone receptors, more aggressive cancer w/fewer treatments.

Question 39

What are some treatments for HPV, is treatment always needed, why/why not?

Answer 39

HPV is a viral STI. Usually pt are asymptomatic, further spreading the disease. No treatment specifically but there is a vaccination available for both men and women. -HPV also causes genital warts, cervical dysplasia, cervical cancer, penile cancer (35%), and 95% anal cancer. -Genital warts (condylomata acuminata) usually resolves on its own.

Question 40

What are the different types of STI’s and their s/s; how are they treated and which one is the most prevalent

Answer 40

Condylomata acuminata (genital warts) -caused by HPV (fastest growing STI) -transmitted direct skin-skin -mother to newborn -usually resolve by itself -no treatment just vaccine Genital herpes -caused by herpes simplex virus -highly contagious -only 2/8 sexually transmitted (hsv1/2) -spread by contact w/infectious lesions but also spread when no lesions/symptoms present -incubation 2-12 days INITIAL S/S tingling, burning, itching, pain in genital area lesions rupture on day 5 to form wet painful ulcers, crusts over in 10-12 days.

Question 41

What is Peyronie disease, its cause and s/s?

Answer 41

deposition of fibrous CT, a fibrous layer of plaque under Tunica albuginea. During an erection it's an abnormal bowed erection. They can be painful and make intercourse difficult.

Question 42

What is cryptorchidism and its possible consequences?

Answer 42

Failure of one or both testes to descend during the developmental process during latter part of pregnancy. Normally during the last trimester of pregnancy, the testicals will descend through the inguinal canal & into the scrotum. If they fail to descend at their first pediatric appointment, they will palpate the testes and if they have not descended, they will wait and see if they do. If they do not, they will surgically bring them down. -may be due to small inguinal ring or endocrine abnormalities -if the testes are left in the abdominal cavity, testes may be nonfunctional and increase risk of being cancerous.

Question 43

What is spermatocele, hematocele, hydrocele, variocele, testicular torsion?

Answer 43

Spermatocele: cyst w/fluid and sperm around testis, due to abnormality of seminiferous tubules. Hematocele: accumulation of blood around testes + scrotum, causing the scrotal skin to become dark red or purple. Due to trauma, bleeding disorders, or testicular tumor Hydrocele: excess fluid around testes, often congenital and can develop following an injury. Overtime the fluid will spontaneously reabsorb. Varicocele: dilated vein in scrotum spermatic cord, due to lack of valves in veins after puberty. Normally happens following trauma, bc of anatomical difference where scrotum vein originates (L. side). Since dilated in vein in testes, temperature of testes (primary sex organ) increases, may cause low sperm count. Testicular torsion: testis rotates on spermatic cord after trauma or spontaneously. This causes blood flow to that testes decrease. This is a medical emergency and requires surgery. If too much time between onset of symptoms & unwinding (resolving testicular torsion), testicle will die, and no sperm will be produced. ER: will use a doppler to see if any blood flow is going to testicle, if not they will try external manipulation to unwind it, but most likely will perform surgery.

Question 44

In what zone of the prostate does cancer develop, does hypertrophy occur in. What is some s/s of BPH?

Answer 44

Hypertrophy- transitional zone prostate cancer - peripheral zone S/S -50+ -hard nodule detected by digital exam -urinary hesitancy -prostate specific antigen test, 45+

Question 45

What is orchitis?

Answer 45

infection/inflammation of the testes caused by mumps - more serious in adults than children due to having decreased sperm count, which may cause infertility.

Question 46

What is prostatitis and what are the different types of prostatitis

Answer 46

Inflammation of the prostate gland, may or may not show s/s. Types of prostatitis -Asymptomatic inflammatory [Acute bacterial] subtype of UTI impaired IS, recent catheteri strictures, fevers, chills, myalgia, arthalgia, swollen, tender prostate via digital rectal exam, joint pain [Chronic bacterial] pt's w/ recurrent UTI frequent urgent, dysuria, perineal discomfort, lower back pain Chronic Nonbacterial Prostatitis Chronic prostatitis Inflammatory: elevated leukocytes in prostatic fluid Noninflammatory No evidence of UTI Men present with s/s including pain along the penis, testicles and scrotum, painful ejaculation, lower back pain, rectal pain, blood in urine/semen

Question 47

What possible consequences might an adult male have if he contracts mumps?

Answer 47

decreased sperm count, infertility

Question 48

What is hypospadias, epispadias and how is it treated

Answer 48

Hypospadias: urethral opening is not at the tip of the penis, but the ventral side. Fixed by surgical reconstruction. Epispadias: urethral opening on the upper/distal surface, proximal to the glans -> incontinence may result. Fixed by surgical reconstruction.

Question 49

What is phimosis and paraphimosis; how are they treated

Answer 49

Phimosis: inability to retract foreskin. Tightening of the foreskin where it cannot fully retract. Treated by circumcision to remove the foreskin or stretch it. Paraphimosis: foreskin trapped behind the glans penis -> can restrict blood flow to the glans penis causing ischemia and necrosis. Medical emergency. Treated by circumcision.

Question 50

What are some s/s of testicular cancer

Answer 50

They may be no symptoms. If symptoms occur, -discomfort/pain in the testicle, feeling of heaviness in scrotum -dull ache in back or lower abdomen -hard painless mass, enlargement of a testicle or a change in how it feels -excess development of breast tissue (gynecomastia)- this also can develop normally in adolescents does not = cancer -lump/swelling in either testicle

Question 51

What are some s/s of ankylosing spondylitis

Answer 51

It is a chronic progressive inflammatory condition that affects the sacroiliac joints, intervertebral spaces + costovertebral joints. S/S kyphosis initial lower back pain, stiffness pain more pronounced when lying down mobility decreases (flex, ext, rotation) as calcification develop, spine rigid,

Question 52

What is the difference between reactive arthritis, osteoarthritis and psoriatic arthritis?

Answer 52

Reactive arthritis: joint is inflamed, but there is no pathogen in the joint causing it. Normally seen following an infection/STI -can't see due to conjunctivitis -can't pee -> nongonococcal urethritis/cervicitis -can't climb a tree -> bladder/urethra Osteoarthritis: most common arthritis "Degenerative joint disease" [Idiopathic/primary] happens as we age [Secondary] congenital/acquired -> trauma, metabolic disorders, inflammatory disease Caused by wear and tear on the joint. As we age, we lose some articulated cartilage, have bone rubbing on bone in the joints. As articulating cartilage is broken down, osteophytes form, 'bone sturs'. Reason for damage bc when ur releasing chemicals (cytokine), increasing protease activity, it destroys articulate cartilage and breaks down the protein making the joint. Cartilage no longer protects the bone. Psoriatic arthritis: Genetic, environmental, immunological factors appear to be involved -> T cell mediated immune response. Seen in people w/psoriasis. 5 subgroups -Oliarticular form - 4 or fewer joints Spondylitis form- sacroiliitis, spinal involvement Polyarticular/symmetric - most common form, resemble RA Distal interphalangeal joint is affected arthritis mutilans - very destructive

Question 53

What causes gout and how is it treated; how do the treatments work? ('Gouty arthritis')

Answer 53

Happens due to a buildup of uric acid crystals in the joint. First the big toe joint is affected. As blood circulates around the foot, blood comes close to the surface, cools down & uric acid crystals come out of solution and get deposited into the joint. Accumulation of these uric acid crystals (Tophi), causing inflammation on the joint, -Developed by overproduction of UA and under secretion of UA. -UA crystals could block the renal/kidney tubules and cause kidney stones. Treatment NSAID- pain Colchicine - prevents the macrophages from reaching the site, decreases inflammation xanthine oxidase inhibitors including allopurinol and febuxostat → limit the amount of uric acid your body makes, blocks the conversion/limits the amount of UA your body makes, decreasing amount of UA. * Probenecid improves your kidneys' ability to remove uric acid from your body. Increases excretion of UA by the kidneys.

Question 54

Describe the different types of fractures

Answer 54

Complete: broken into two or more pieces * Incomplete: partly broken, incomplete fracture → greenstick fracture (results from bending of short bone in children) * Open: fracture resulting when skin in broken → soft tissue damage, nerve damage, blood vessel damage. Higher risk of infection -takes skin * Closed fracture: Skin is not broken. Bone does not come through the skin Occult: normal s/s of fracture, but nothing appears on XRAY. Transverse: a straight horizontal break across bone Oblique: a diagonal break across the bone H. Greenstick: a partial fracture where the bone bends, common in children. Displaced: bone out of place Nondisplaced: bone in place

Question 55

Number of fracture lines on bone

Answer 55

Simple: single break in which bones maintain alignment. Compression: multiple vertebrae in the spine are broken Comminuted: bone is broken, splintered, or crushed into a number of pieces

Question 56

What is the difference between a Potts, Smith and Colles fracture

Answer 56

Colles' fracture: break in distal radius of wrist (extends arm to break fall). Or if a person pushes you instead of stopping the fall by pushing palms out, they face you & fall on your wrist -> smith fracture, more severe damage to nerves than Colles Potts fracture: lower fibula due to excessive stress on ankle (stepping down) -walk downstairs and think that you're at the bottom but you're not -ankle distal fibula

Question 57

6 P's of fracture complications

Answer 57

Pain Pallor Pulselessness Paresthesia Paralysis Poikilothermiea (change in temp above or below break)

Question 58

What is the difference between a sprain and a strain?

Answer 58

Sprain is a tear in a ligament Strain is a tear in a tendon

Question 59

What is rickets and its causes

Answer 59

Failure of the bone to calcify. It is seen in children. 'Soft bones' [Nutritional rickets] not intaking proper nutrition (vitamin D, Ca+2, P) /sunlight to form and adequately mineralize the bone. [vitamin D-dependent rickets] mutations in enzyme for active vitamin D or receptor [Vitamin D- resistant rickets] mutations resulting in decreased serum phosphate

Question 60

What is osteoporosis, how can it be prevented and how is it treated?

Answer 60

A significant loss of calcium to the bone. It is a metabolic bone disorder that results in decreased bone mass/density. Bone reabsorption exceeds bone formation. [primary] postmenopausal; estrogen is needed for osteoblast activity and when women go through menopause their estrogen will decrease, osteoblast activity will decrease, clast activity will increase [2ndary] occurs following primary disorder like Cushing's syndrome; increased clast activity, decreased blast activity After a certain amount of bone demineralization in osteopenia (loss of ca), it progresses to osteoporosis. Treatment/prevent Calcium + vitamin D supplements Bisphosphates - inhibit clast activity Calcitonin (stimulate blast activity) +parathyroid hormone =breaks down bone to stimulate bone turnover and deposition of new calcium in bone. Weight baring exercise Hormone replacement therapy (estrogen) - if severe

Question 61

What is rhabdomyolysis and what cause it?

Answer 61

When a muscle is damaged, a protein pigment called myoglobin is released into the bloodstream and filtered out of the body by the kidneys. Myoglobin breaks down into potentially harmful compounds. It may block the structures of the kidneys, causing damage such as acute tubular necrosis or kidney failure. -coca cola urine (myoglobin in urine) -Since cells are damaged, Phosphate and Potassium leak out. Results in hyperkalemia + hyperphosphatemia. Hypocalcemia. -2nd cause = excessive exercise

Question 62

What are the different stages of bone healing

Answer 62

1) Bleeding clot forms (hematoma), forms the 1st fibrous network. 2) New vessels going to come into the area bring the phagocytic cells, neutrophils, macrophages, and will clean up the site of the broken bone. They will remove all splinters, necrotic tissue so healing can occur. 3) Fibroblasts will enter area, lay down fibrous tissue & transition into chondrocytes to lay down cartilage. The osteoblasts will migrate into soft callus from the adjacent region and begin to lay down osteoid (organic part of bone) osteoid makes up the soft callus (immature bone not calcified), 2 ends of the bone now splintered together. 4) After the soft callus has been formed, the bony callus will begin building where osteoid gets mineralized w/Calcium + phosphate. After the bone is mineralized, you can take the cast off. Remodeling occurs. The bone has to be immobile until a hard callus is formed. Remodeling occurs in response to mechanical stress on the bone.

Question 63

What factors promote bone healing, delay bone healing

Answer 63

Factors affecting healing -amount of local damage -gap side between broken ends: must keep immobile to ensure proper healing -secondary problems; infection, or foreign materials at site -Age, circulatory issues, nutritional status, other disease process (anemia)

Question 64

What is compartment syndrome, what can cause compartment syndrome

Answer 64

An increase in pressure in muscles due to damage being done. Muscle gets inflamed and gets surrounded by CT (fascia) which prevents the muscle from swelling outside the boundaries created by the fascia. This leads to Compartment syndrome -> greater tissue damage & necrosis due to decreased blood flow. caused by prolonged, continuous pressure on a body part

Question 65

What is Paget’s disease and its s/s

Answer 65

A progressive bone disease seen in adults over 40. Focal areas of excessive osteoclast activity, where osteoblasts respond by trying to throw the Calcium back into the bone, but in a disorganized manner. The new bone formed by the osteoblasts because of the loss caused by excessive overactivity of osteoclasts is disorganized and results in deformities. -overactive clasts and blasts try to keep up S/S regions of excessive bone turnover new bone is disorganized deformation, fractures common bone expansion - due to way the osteoblasts are laying down calcium in response to excess osteoclast activity, easy to fracture, frequent fractures, weak bones fractures - although bone affected by this condition usually expand, it is weaker than usual and more likely to break than normal healthy bone

Question 66

Understand the pathophysiology, etiology, s/s, treatments (if any) for rheumatoid arthritis

Answer 66

Autoimmune disorder where the body makes antibody that attack the joints in hands + feet. It can affect any of the synovial joints + inflammation of synovial membrane which results in destruction of the joint architecture. -Bone broken and held in place by abnormal calcification -Dangerous granulation tissue (Pannus) results in loss of cartilage and erode the bone. -Possible genetic predisposition to rheumatoid factor, a group of antibodies present in the circulation of people w/ RA. S/S swollen knuckles deformed fingers ulnar deviation subcutaneous nodules Treatments NSAIDS/ COX-2 inhibitors - pain Corticosteroids - decrease inflammation Disease modifying antirheumatic drugs - suppress overactive IS Biologic agents