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PATHOPHYS-2 2ND HALF
Male Repro, Female Repro, Endocrine, Neuro, Derm
| Question | Answer |
|---|---|
| Psychogenic causes of ED | PA (perf anx-- not Prince Albert), strained relationship, depression, psychosis |
| "Organic" causes of ED | neurogenic, hormonal, vascular, drug side-effects, mechanical/anatomical |
| Erection (involuntarily) lasting more than 4-6 hours | priaprism |
| Causes of primary priaprism | malfunction in the blood vessels and the nerves in the penis |
| Causes of secondary priaprism | misuse of ED meds. Some antidepressant and anxiolytic medications may also cause priapism. Blood thinners and other HTN drugs may also sometimes cause the condition |
| Risk factors for penile cancer | Old age, smoking, HPV, UV exposure, "AIDS patient." Shahid is obsessed with genital hygiene so add uncircumcised & poor foreskin washing. |
| Disorders of scrotum & testes | crytpoorchidism, hydrocele (fluid in tunica vaginalis), hematocele (blood in tunica vaginalis), spermatocele (sperm CYST in the epididymis), variocele (varicosities of pampiniform plexus of veins supplying the testes), testicular torsion, epididymitis |
| Cryptoorchidism consequences | sterility (95% of cases). But also 6-fold increased risk of malignancy. (Also possible psychological effects of empty scrotum). |
| Classify testicular tumors. | Stage 1= confined to testes, epididymis, spermatic cord. Stage 2=spread to retroperitoneal LN and BELOW DIAPHRAGM. Stage 3=spread beyond retroperitoneal LN or above diaphragm |
| Which testicular tumors are most common? | GERM CELL IN ORIGIN (as opposed to sex cord/gonadal stroma) |
| What may be a special manifestation of Leydig cell tumor? | they often produce either testosterone or estrogens, and their presence can cause PRECOCIOUS PUBERTY in pre-adolescent males |
| What are the causative organisms of acute bacterial prostatitis? | usually E. coli (but others include pseudonomas, klebsiella, and proteus) |
| What are the symptoms of acute bacterial prostatitis? | fever & chills, "irritative" voiding symptoms (frequent, urgent, painful), dull rectal or perineum pain, swollen, tender, warm prostate on digital exam. (Urinalysis shows pyuria, bacteriuria, hematuria.) |
| What are the characteristics of benign prostatic hyperplasia (BPH)? | large, discrete lesions in the PERIURETHRAL region of the prostate (NOT peripheral zones-- these are affected by prostate CANCER) |
| What is the pathology of benign prostatic hyperplasia (BPH)? | "truly a hyperplastic process": hyperplasia of GLANDS (epithelium) + increased fibromuscular STROMA |
| What are the hormonal influences of carcinoma of the prostate? | testosterone "plays a role" |
| What are the sites of metastases of carcinoma of the prostate? | local LN and vertebrae, "other bones," internal organs |
| What are the risk factors for carcinoma of the urinary bladder? | Smoking "accounts" for 60% of cases. Exposure to industrial dyes/solvents accounts for 15%. |
| What are the histologic types of carcinoma of the urinary bladder? | 90% are transitional cell carcinomas |
| What are the clinical features of carcinoma of the urinary bladder? | Blood in urine (gross or microscopic), "chronic or intermittent." Most patients fail to have ´signs´ "b/c of its superficial nature" |
| Causes of vaginitis in premarchal women? | Usually bugs or FB :) |
| Causes of vaginitis in WOCBA? | Candida (fungus), trichomonas (fungus), gardnerella (bacteria) |
| Causes of vaginitis in PMM? | atrophic vaginitis ;( |
| Characteristics of cervical polyps | Red velvet cupcakes (but hanging like grapes) |
| Symptoms of cervical polyps | post-coital bleeding and/or spotting between periods |
| Incidence of cervical polyps | MOST COMMON CERVICAL LESION |
| Treatment of cervical polyps | Excision and examination |
| Risk factors for cervical cancer | Total life time "activity"/exposure down there, so: start early (pregnancy, marriage), lots of pregnancies, lots of partners (or partner with lots of partners), OC, HPV. Also smoking and immunosuppression. |
| Clinical features of cervical cancer | intra-epithelial neoplasia typically preceeds frank cancer (by 15 years). Cervical cancer can be ASYMPTOMATIC. Or there can be post-coital bleeding. |
| Dx procedure for cervical cancer | Pap smear |
| Endometritis | Inflammation or irritation of the lining of the uterus (endometrium) d/t chlamydia, gonorrhea, or other bacteria |
| Endometriosis | the presence of endometrial tissue outside of the uterus (typically on the ovaries, FTs, or within the peritoneal cavity or cul de sacAdn) |
| Adenomyosis | uterine thickening that occurs when endometrial tissue (GLANDS & STROMA) moves into the outer muscular walls (MYOMETRIUM) of the uterus |
| Leiomyoma | aka fibroids= benign neoplasm of smooth muscle tissue origin. "Most common pelvic tumor" |
| Pathogenesis of endometriosis | Suspected to involve "retrograde" or regurgative menstruation (up and out the FTs and into the peritoneal cavity) |
| How to dx endometriosis | Triad of symptoms: pain at menstruation, pain at intercourse, infertility. THE ONLY METHOD OF ACCURATE DX IS LAPAROSCOPY. |
| Manifestations of 3 types of leiomyomas | INTRAmural and SUBserosal typically cause only pressure/pain, but SUBmucosal more likely to cause BLEEDING, necrosis and infection. |
| Complications of 3 types of leiomyomas | Subserosal (and intramural) tumors can compress the rectum and urinary bladder. Submucosal tumors tend to grow into endometrial cavity and cause menstrual irregularities and endometrial BLEEDING (necrosis & infection). |
| Name the 3 tyypes of leiomyomas | SUBmucosal, SUBserosal, INTRAmural |
| Most common form of pelvic tumor | MYOMA/LEIOMYOMA (of the 3 tyypes, INTRAmural is most common) |
| Lesion caused by HSV2 | painful, recurrent, grouped blisters on the VULVA or PERIANAL skin |
| Lesion caused by HPV | genotypes 6 and 11 produce labial, vaginal, cervical warts (condylomae) |
| Lesion caused by syphilis | primary syphilis produces vulvar or penile CHANCRE |
| Chancre | usually occurs (penis, labia, cervix, anorectal area) 3 weeks after syphilis infection; it is a single, red papule that gradually begins to erode, forming a painless, clean ulcer with a smooth, raised border. (Extragenital sites include lips and tongue!) |
| Risk factors for PID | swinging, young single chick: >24 years old, multiple partners, no live births. (also history of PID, but that's kind of a DUH) |
| Potential complicatios of PID | Fallopian tubes become red, swollen, pus filled. Tubo-ovarian ABSCESS may develop as infection spreads to ovaries. PERITONITIS may result. Other risks/complications include INFERTILITY and ECTOPIC PREGNANCY. |
| Most common site for ectopic pregnancy? | The F tubes |
| Predisposing factors for ectopic pregnancy? | PID, history of ectopic pregnancy, use of fertility drugs to induce ovulation, morning after pill or failed contraception. Other weird things on list: therapeutic abortion, tubal ligation or reversal, intrauterine exposure to DES, "infertility." |
| Manifestations of PCOS? | menstrual irregularities, infertility, virilization/hirsutism (all brought on by hormonal disturbances). LH levels will be high, with normal FSH and estrogen numbers. |
| Pathogenesis of PCOS? | Hormonal d/o or the H-P-O axis with pathologically enlarged ovaries studded with (follicular) cysts |
| Most common GYN cancer? | UTERINE (endometrial) CANCER IS #1!! (ovarian cancer is #2-- but OVARIAN cancer is #1 cause gyn cancer cause of death) |
| Significance of Krukenberg tumor? | is a metastasis from cancer SOMEWHERE else in the body (most often from stomach cancer, but sometimes also intestine or even breast)-- to the OVARIES!! |
| Physical symptoms of PMS | Painful, swollen breast, bloating/ab pain, headache/backache |
| Psychologic symptoms of PMS | Depression, irritability, anxiety, "behavioral changes" |
| Causative agent of acute mastitis? | Pyogenic bacteria (most often Staph aureus) |
| How common is fibrocystic breast disease? | MOST FREQUENT "LESION" OF THE BREAST |
| What are the pathological changes in fibrocystic breast disease? | fibrosis and cyst formation |
| What are the manifestations of fibrocystic breast disease? | Pain, nodularity, (often extreme) sensitivity upon palpation |
| What is the age distribution for fibroadenoma of breast? | Found in women from 15 to 35 ("most common benign tumor of the breast") |
| What are the examination findings for fibroadenoma of breast? | "well-encapsulated mass, 2-5 cm in diameter," solitary and freely movable (composed of fibrous stroma & glandular epithelium). Easily removed surgically-- and does not recur. |
| Risk factors for breast cancer? | Genetics factors (BRCA1/2 mut), white race>AA>Asian, family history, increased lifetime exposure to estrogen (=early menarche, late menopause, no kids, late first kid, HRT, high fat diet), BREAST IRRADIATION (!!), old age, other cancers (ovarian, uterine) |
| Clinical presentation of breat ca? | Possible mass on palpation, smaller tumor by mammography, possible mastodynia (although Shahid initially said "cancers do not create pain"). Late stage c/b nipple retraction, "eczematoid reaction," discharge |
| Causes of male infertility? (one set of answers) | Problems with sperm (azoospermia (no sperm), oligospermia (small amount), asthenospermia (sperm not feeling well) |
| What are the causes of male infertility? (a second set of answers) | variocele, ejac dysfx, HYPERprolactin, HYPOgonadism, infection, anti-sperm Abs, obstruction, congenital abnormalities |
| Hallmarks of pre-eclampsia | HTN, edema, proteinuria |
| Hallmarks of eclampsia | HTN, edema, proteinuria, SEIZURES |
| Causes of hyperthyroidism | Autoimmune (Graves'), goiter, tumor (thyroid adenoma), misuse of thyroid replacement hormones (factitious thyrotoxicosis) |
| Manifestations of hyperthyroidism | Irritability, anxiety, restlessness, heat intolerance, increased sweating. Tachycardia, palpitations. Increased appetite, diarrhea, weight loss. Thin, silky hair and skin. Dyspnea. |
| Etiology of Graves' disease | autoimmune d/o caused by abnormal stimulating of thyroid by Abs |
| Precipating factors for thyroid storm | stress, DKA, thyroidectomy |
| Manifestations of Graves' disease | bulging eyes, swollen tibial crests, enlarged thyroid |
| Manifestations of thyroid storm | VERY HIGH FEVER. Tachycardia/angina. SEVERE CNS EFFECTS (agitation/delirium) |
| Consequences of the hyperCa* in hyperparathyroidism | Calcification of soft tissue. Kidney stones. Heart electrical problems. Muscle weakness. |
| Manifestations of hyperparathyroidism | Stones, bones, moans, groans |
| Causes of Cushing's (syndrome) | adrenal tumor, ectopic production of ACTH by small cell lung carcinoma. WIKIPEDIA SAYS... most common cause of Cushing's syndrome is exogenous administration of glucocorticoids used to treat other diseases such as asthma, RA, or after an organ transplant. |
| Manifestations of Cushing's syndrome | moon face, buffalo hump, muscle (limbs) wasting, osteoporosis, central obesity |
| Pathophysiology of adrenogenital syndrome | congenital deficiency of enzyme necessary for synthesis of cortisol (this results in excess production of ACTH and then excess production of adrenal androgens) |
| Manifestations of adrenogenital syndrome | freakishly large penis in baby boys, ambiguous genitalia bodering on hemaphroditism in baby girls |
| What are the manifestations of adrenocortical hypofunction (Addison’s disease)? | "Addled" by fatique, nausea/diarrhea, weight loss, hypotension, syncope, hyperpigmentation of skin ("fadded pig") |
| What is pheochromocytoma? | (literally, "dusky color growing cell") Usually a benign tumor of MEDULLA of adrenal glands IN ADULTS. (Dx´d by "vanilla" acid in urine: VMA). There can be paroxysmal HTN. |
| Compare the characteristics of diabetic ketoacidosis (DKA) and hyperosmolar hyperglycemic state. | DKA is an acute complication of, mostly, Type 1. HHS is an acute complication of, mostly, Type 2. |
| Compare the characteristics of diabetic ketoacidosis (DKA) and hyperosmolar hyperglycemic state. | DKA is overproduction of ketones (which are acidic) by the liver as it breaks down fats for fuel (instead of sugar-- since there is no insulin). Hyperosmolar hyperglycemic state is hyperosmolarity of the blood d/t extremely high levels of GLUCOSE in it. |
| What is the pathogenesis of polyuria, polydipsia, and polyphagia in diabetes mellitus? | Too much sugar in blood tells KD to pee, pee, pee. That results in dehydration/thirst. The "big appetite" comes from "abnormal utilization of protein/carbs/fats" (because there is no insulin to break down sugar) |
| What is the pathogenesis of retinopathy in diabetes mellitus? | "Microangiopathy" of retina leads to microaneurysm, hemorrhage and ischemia/infarct (of retina) |
| Define stroke | interruption of blood flow to cerebral vessel |
| Casues of ischemic stroke | THROMBUS (usually in atherosclerotic vessel) |
| Causes of hemorrhagic stroke | HTN, aneurysm, arteriovenous malformation (hemorrhagic stroke is bleeding into brain tissue from a ruptured BV) |
| Risks for cerebral aneurysm | Polycystic kidney disease, coarctation of aorta |
| Define cerebral aneurysm | Abnormal bulge or ballooning of a BV supplying the CEREBRUM (typically at arterial bifurcations) |
| What is the pathophysiology of multiple sclerosis? | immune medicated inflammatory disease that attacks myelinated axons of the CNS |
| What are the MRI findings in multiple sclerosis? | "periventricular plaques," as well as multiple focal demyelination in brain & spinal cord |
| What are CSF findings in multiple sclerosis? | increased levels of IgG in many patients |
| What are the pathophysiological processes involved in Alzheimer’s disease? | loss of neurons and synapses in cerebral cortex and some subcorticoid regions |
| How do β-amyloid proteins contribute to the pathology of Alzheimer’s disease? | deposition and aggregation of beta amyloid proteins lead to neuronal death |
| How do neurofibrillatory tangles contribute to the pathology of Alzheimer’s disease? | NFTs are aggregates of hyperphosphorylated tau protein, In its hyperphosphorylated state, the tau protein is unable to bind to the microtubules and they become unstable and begin disintegrating. |
| Which neurotransmitter is DECREASED in the CNS in Alzheimer’s disease? | acetycholine |
| What are the manifestations of early stage Alzheimer’s disease? | loss of short-term memory, problems with word finding, mood swings, personality changes. Agnosia (problems identifying objects). Apraxia (problems performing previously learned motor activities). Aphasia (impaired ability to use or comprehend language). |
| What are the manifestations of late stage Alzheimer’s disease? | Inability to perform the tasks of daily living. Inability to walk. Inability to feed oneself. Complete loss of short- and long-term memory. Incontinence. Inability to swallow. Could eventually become mute. |
| What are the screening tests for Alzheimer’s? | short-term memory test (also "formal mental state examination") |
| What are the diagnostic tests for Alzheimer’s disease? | LAB: Complete Blood Count, Liver Funtion Test (??), Thyroid Stimulating Hormone, B12 levels RADIOLOGY: CT or MRI (to rule out other causes) |
| What are the bacteria that most commonly cause meningitis in neonates? | Staph agalactiae, Listeria, E. coli |
| What are the bacteria that most commonly cause meningitis in adults? | Staph pneumoniae |
| What are the CSF pictures of bacterial meningitis? | the bacteria feed on sugar, so GLUCOSE levels greatly reduced. Neutrophil (and protein) counts elevated. (Makes sense since neutrophils would multiply to fight off bacterial pathogen.) |
| What are the CSF pictures of viral meningitis? | increase in B lymphocytes ("mononuclear cells"). Makes sense since B cells make Abs. Protein levels may or may not be elevated. Glucose normal. |
| What is amyotrophic lateral sclerosis (ALS)? | loss of lower motor neurons of spinal cord/brain stem and upper motor neurons of corticospinal tracts. Degeneration of upper and lower motor neurons leads to muscle weakness and atrophy through the body. |
| What is "a known cause" of ALS? | 5-10% of cases familial (fALS), autosomal dominant. (25% of these are caused by mutation of SOD1 gene in Chromosome 21!) |
| What is the genetic basis of Huntington disease? | a trinucleotide repeat disorder (CAGCAGCAGCAG). Instead of a single glutamine (CAG), you end up with a "polyglutamine tract." >36 repeated CAG sequences --> cytoplasmic protein Huntington; >36 repeated CAG sequences --> mHtt. |
| What are symptoms of Huntington disease? | CHOREA: jerky, hyperkinetic, sometimes dystonic movements involving all parts of the body |
| What is the pathophysiology of Huntington disease? | atrophy of the CAUDATE NUCLEUS and PUTAMEN (of basal ganglia) |
| Give examples of prion diseases. | In humans, Creutzfeldt-Jakob Disease (CJD and vCJD) and (in Central Africa and New Guinea) kuru. In cattle, Bovine Spongiform Encephalopathy (BSE). |
| Which prion disease is the most common? | CJD |
| What is the pathogenesis of prion diseases? | Problem with PrP protein in neurons: presence of abnormal "beta-pleated sheet" instead of normal alpha-helix isoform. The mutated form is resistant to "diegestion" by proteases, and accumulation of PrP in neural tissue (and DEMENTIA) ensue. |
| What are the causes of neural tube defects? | Some vertebrae overlying the spinal cord are not fully formed and remain unfused and open. If the opening is large enough, a portion of the spinal cord can protrude out through the opening in the bones. |
| What are the different types of spina bifida? | oculta, cystica with meningocele (just meninges protudes out), cystica with myelomeningocele (both meninges AND spinal cord protrude out) |
| Classify CNS tumors. | Primary ("true") and secondary |
| What are the three main categories of brain tumor? | glioma, meningioma, pituitary adenoma (PAMG) |
| What are the (three main) consequences of brain tumor? | intracranial HTN, dysfunction, irritation (abnormal fatigue, tremors, seizures) |
| What are the risk factors for carpal tunnel syndrome? | RA, DM, hypothryroidism, ACROMEGALY!, pregnancy, repetitive Flex/Ext of wrist |
| What are the most common causes of polyneuropathy? | autoimmune (Guillian-Barré), poisoning (lead, arsenic, ETOH), metabolic (DM, uremia) |
| What is the etiology of Gullain-Barré syndrome? | Autoimmune (thought to be triggered by infection, surgery, vaccination, campylobacter or other diarrheal pathogens, herpes viruses, mycoplasma) |
| What is the pathology of Gullain-Barré syndrome? | "infiltration of MONONUCLEAR CELLS around the capillaries of PERIPHERAL NEURONS and subsequent demyelination of VENTRAL SPINAL NERVE ROOTS |
| How is Gullain-Barré syndrome diagnosed? | Ask about possible triggers in recent past. Look at CSF for super elevated protein level? |
| What are the manifestations of autonomic neuropathy in long-standing diabetes mellitus | GI and GU disturbances" GI= gastroparesis w/ delayed gastric emptying and NOCTURNAL DIARRHEA! GU= neurogenic bladder, impotence in men. Also orthostatic hypotension leading to postural syncope, dizziness/lightheadedness. |
| What is the pathophysiology of myasthenia gravis? | autoimmune disorder of the NEUROMUSCULAR JUNCTION |
| What are the symptoms of myasthenia gravis? | episodic muscle weakness and/or quickly fatigued muscles (even talking, chewing) |
| How is myasthenia gravis diagnosed? | "TRIAL OF EDROPHONIUM" (IV infusion that temporarily blocks the Ab/T-cell attack on the acetylcholine receptors). ACH-receptor Abs present in many pts. |
| Most important skin carciongen | UV rays (sun) |
| Causes of bullae formation on the skin | sunburn? |
| Macule | flat, slightly hyperpigmented skin lesion (patch) less than 1 cm (FRECKLE) |
| Papule | slightly elevated skin lesion (ALLERGIC ECZEMA) |
| Vesicle | fluid filled elevation of epidermis (cold sore on lip) |
| Bulla | a large vesicle (burns) |
| Pustule | pus filled vesicle less than 1 cm (IMPETIGO) |
| Ulcer | discontinuity of skin showing complete loss of epidermis (CHANCRE) |
| Scale | keratin layers or flakes covering the skin (PSORIASIS, SEBORRHEIC KERATOSIS) |
| Effects of sun on skin | hyperemia (increased blood flow to the area), 1st and 2nd degree burns |
| Appearance of rash in impetigo | Honey Crusted Lesions |
| Appearance of measles rash | maculopapular rash (brick red) |
| Koplik's spot | whitish patches near parotid duct (at 2nd molar) just before measles outbreak |
| HSV2 outbreak on labia or genitals | recurrent, grouped, small vesicles on erythematous base (RGSVOEB) |
| Which one had the SPAGHETTI & MEATBALLS ? | Tinea versicolor (think of the red color of the sauce?) |
| And the cottage cheese? | candida albicans |
| Pathogenesis of acne | androgen overproduction of keratin AND sebum (and then feeding on sebum by bacteria whose 'waste products' are pro-inflammatory fatty acids (omega 6?)) |
| Factors contributing to acne | androgen surge and hypertrophy of sebaceous glands |
| What are the lesions of acne (vulgaris)? | inflammatory (teenage acne) and non-inflammatory (black heads, white heads) comedones |
| How does seborrheic dermatitis (aka dandruff) typically present? | Reddening, scaling, itching (scalp, nasolabial folds, eyebrows) |
| What is the appearance of the lesions of psoriasis? | red plaques covered with SILVERY SCALES (extensor aspect) |
| What is the appearance of seborrheic keratosis? | wartlike lesions with "stuck on" appearance. Loosely attached and easily removed |
| Name the skin tumors. | There are 3. The bad ones are BCC and SCC. The benign one is the "wartlike lesions with stuck on appearance": seborrheic keratosis |
| What is most common epithelial malignant tumor of skin? | the BBC (BCC) |
| What is the appearance of basal cell carcinoma? | remember that the BBC HQ is a round building with an open courtyard in the center: "Slightly elevated nodule with central depression." |
| What is the HALLMARK of basal cell carcinoma appearance under microscope? | blood vessel like "telangiectactic nodules" at its center |
| What is the pathogenesis of skin cancer from chronic exposure to sunlight? | Capacity of DNA repair enzymes is overwhelmed by the task at hand. Faulty or incomplete DNA repair results in unchecked cell growth. |
| What is the appearance of actinic keratosis? | Flesh-colored skin lesions (plaques) on sun exposed areas that FEEL LIKE SANDPAPER and are TENDER when the finger is drawn over them |
| What is the significance of actinic keratosis "lesions?" | AK can become SCC (sandpaper lesions on face hands get SACCK'd) |
| Name pigmented (of melanocytes) skin lesions. | Lentigo, nevus, malignant melanoma |
| Which pigmented lesion of the skin is likely to progress to malignant melanoma? | Dyplastic nevi (mole that starts to grow, especially irregularly) |
| What are the diagnostic criteria for malignant melanoma? | A-B-C-D. A for asymmetry. B for irregular borders. C for color change. D for increase (>6mm should cause concern) in diameter |
Created by:
mrbarr
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