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SIUE Patho Test III
Patho Test III
| Question | Answer |
|---|---|
| How will labs appear in SIADH | Serum HYPOosmolarity (<280), HYPOnatremia (<135), Urine HYPERosmolarity, Urine sodium that matches sodium intake, Normal Renal/Adrenal/Thyroid Function |
| What causes SIADH? | oversecretion of ADH leads to reabsorption of water by the renal collecting duct; leads to dilutional hyponatremia. |
| Clinical Manifestations of SIADH with rapid decline of Na+ from 140 to 130 | Fatigue, DOE, Thirst, impaired taste, anorexia, dulled sensorium, no peripheral edema |
| Clinical Manifestations of SIADH with decline of Na+ to 130-120 | Vomitting and abdominal cramps |
| Clinical Manifestations of SIADH with decline of Na+ to 115-110 | confusion, lethargy, muscle twitching, convulsions, severe sometimes irreversible brain damage |
| What is DI? | Insufficiency of ADH that leads to polydipsia and polyuria. It is a partial or total inability to concentrate urine. |
| What are the 2 types of DI? | Neurogenic and Nephrogenic |
| Describe Neurogenic DI and risk factors | Also referred to as central DI. Caused by insufficient production of ADH by the hypothalmus. Can be caused by neurosurgery or brain truama |
| Describe Nephrogenic DI and risk factors | The renal collecting duct is insensitive to ADH. Can be caused by genetic factors or kidney diseases. |
| How differentiat DI from Other diseases | In DI during a water deprivation test, the patient will continue to urinate large volumes, where as other disease processes will show a decline in urination following water deprivation. |
| DI Labs | Serum HYPERosmolarity, Hypernatremia, Urine HYPOosmolarity, decreased urine specific gravity |
| Similarities Between DI, DM, & SIADH | polydipsia, Others? |
| DM I clinical Manifestations | Polydipsia, polyuria, polyphagia, anorexia |
| DM II clinical Manifestations | usually non-specific, but may include polyuria, polydipsia, fatigue, visual changes, paresthesias and weakness |
| Cause of Hyperpituitarism | Pituitary adenoma that arises from the anterior pituitary cells |
| Clinical Manifestations of Hyperpituitarism | Visual Disturbance from optic nerve pressure, increased GH and prolactin, pressure on other anterior pituitarty cells leads to decrease in gonadotropic, THS, and ACTH |
| Lab changes seen in Graves Disease | Increased T3, Increased TH, Decreased TSH, Decreased TRH, Presence of Thyroid Stimulating IgG. |
| How does a Goiter Form in Graves? | Increased metabolism of the thyroid gland leads to hypervacularization and enlargement of the gland |
| Clinical Manifestations of Graves Disease | Pretibial Myxedema, lag of globe on upward gaze or lag of upper lip on downward gaze from overactivity of the eyelid muscles, exophthalmos, vitaligo, pernicious anemia |
| Describe pretibial myxedema | subcutaneous non-pitting swelling on the anterior portion of the leg and indurated erythematous skin |
| What causes exophthalmos | Inflammation and fat accumulation of orbital contents |
| What effects does exophthalmos have on vision? | Causes Diplopia, pain, lacrimation, photophobia, and blured vision |
| Primary Hyperthyroidism | Excess TH secreted by the Thyroid gland. EX.) Graves, toxic multinodular goiter, solitary hyperfunctioning nodules |
| Secondary Hyperthyroidism | Over secretion of TSH by pituitary gland |
| Clinical Manifestations of Hypoparathyroidism | They are related to hypocalcemia. Muscle spasm, hyperreflexia, tonic/clonic seizures, laryngeal spasm, occasionally death from asphyxiation, +Chvostek and Trouseau sign |
| Chvostek Sign | Indicator of hypoparathyroidism (hypocalcemia) Tap cheek and the upper lip twitches |
| Trousseau's Sign | Indicator of hypoparathyroidism (hypocalcemia) Inflate BP cuff to greater than SPB and the patient experiences painful carpal spasm. |
| Hypersecretion of GH in adults | Acromegally, caused by increase GH secretion by the pituitary gland; growth plates are closed, so connective tissue increases in size and bony proliferation occurs, often see arthritis |
| Hypersecrtion of GH in Kids | Giantism |
| Hyperthyroidism Clinical Manifestations | Thin hair, exophthalmos, enlarged thyroid, tachycardia, wt. loss, diarrhea, warm skin, hyperrelexia, pretibial myxedema |
| Hypothyroidism Clinical Manifestations | Loss of hair or coarse brittle hair, periorbital edema, puffy face, normal or small thyroid, bradycardia, constipation, cold intolerance, muscle weakness, extremity edema |
| Increased ACTH Clinical Manifestations | Cushings (thinning of scalp hair, moon face, acne, easy bruising, truncal obesity, skinny extremities, supraclavicular pad, pendulous abd, increased body and facial hair |
| Decreased ACTH Clinical Manifestations | Secondary Hypocortisolism |
| Increased GH Clinical Manifestations | Acromegally in Adults, Giantism in Kids |
| Decreased GH Clinical Manifestations | Dwarfism, fasting hypoglycemia |
| Decreased Adrenal Medulla Function Clinical Manifestations | None |
| Increased Adrenal Medulla Function Clinical Manifestations | HTN, Tachycardia, Diaphoresis (caused by pheochromocytoma) |
| Decreased Adrenal Cortex Function Clinical Manifestations | Addisons disease, weakness, fatigue, anorexia, diarrhea, nausea, hyperpigmentation, vitaligo |
| Increased Adrenal Cortex Function Clinical Manifestations | Feminization of Males or Virilazation of females caused by increased secretion of androgens or estrogens |
| DKA Clinical Manifestations | Malaise, dry mouth, polyuria, polydypsia, wt loss, N/V, pruritis, ABD pain, SOB, Lethargy, Kussmal Resp, Fruity Breath |
| What is most deficient in DKA (compared to HHNKS) | Insulin |
| DKA Labs | BG >250, HCO3 <18, pH <7.3, positive ketones in urine and serum, open anion gap (>12), Increaed Fatty Acids |
| Why does K+ appear normal or increased in the beginning stages of DKA | The K+ shifts out of the cells into the plasma as a result of acidosis, but the overall potassium is really low |
| HHNKS Clinical Manifestations | Polyuria, polydipsia, hypovolemia, dehydration, hypotension, tachycardia, wt loss, ABD pain N/V, Hypothermia, coma, seizures |
| What is most deficient in HHNKS (compared to DKA) | Fluid |
| HHNKS Lab | no ketones, BG >600, Serum Osmol >320, Increased BUN/Cr, pH >7.3 HCO3>15, Glycosuria, decreased free fatty acids |
| Describe DM I | Absolute Insulin Deficiency because of cell mediated destruction of pancreatic beta cells, Patients are insulin dependent, and it is most common in younger population |
| Describe DM II | Insulin resistance with a relative deficiency; usually not insulin dependent, but some patients require insulin, Usually occurs in Fat Old People, Has a strong genetic presisposition |
| Labs that indicate Kidney Damage with DM | Microalbuminuria (30-300mg/day) happens first; protienuria (>300mg/day); Decreased GFR |
| Clinical Manifestations of Cushings | Caused by excessive ACTH; Thinning of scalp hair, moon face, acne, supraclavicular pad, easy bruising, truncal obesity, thin extremities, increased facial/body hair |
| Delayed Puberty | No signs of puberty by age 13 for girls and age 14 for boys |
| Causes of Delayed puberty | Usually just a physiologic delay; may be caused by chronic or systemic conditions (Renal Disease, CF, DM, excessive exercise, anorexia, hematological disease, hypothyroid, IBD, gonadal failure) |
| Cause of primary dysmenorrhea | Release of prostaglandin in ovulatory cycle not associated with pelvic disease |
| Clinical Manifestations of Dysmenorrhea | Pelvic pain that radiates to the back with onset of menses, anorexia, N/V, Diarrhea, Syncope, Head Ache |
| Polycystic Overy Disease Clinical Manifestations | Occurs within 2 years of puberty, hirtuism, Acne, Infirtility, dysfunctional bleeding or amenorrhea |
| PID Cause | Initiated by gonorrhea or clamydia, usually polymicrobial (anaerobes, genital tract mycoplasmas, faculative organisms) Pathogens ascend from infected cervix to infect the uterus |
| Cystocele | Prolapse of the bladder into the vagina; usually occurs during child birth; can lead to incomplete bladder emptying and infection |
| Vaginocele | Herniation projecting into the vagina |
| Rectocele | Prolapse of rectum and posterior vaginal wall into the vaginal canal |
| Cause of Endometriosis | Endometrial cells implant themselves in places where they don't belong (ABD/Pelvic Cavity) |
| Clinical Manifestation of Endometriosis | Infirtility, pain, dysmenorrhea, dyschezia, dyspareurnia |
| Phymosis | Inability of foreskin to retract over the glans |
| Paraphymosis | The foreskin is retracted and cannot be moved over the glans |
| What is the significance of BRCA1 | Presence of this gene increases an individual's risk of breast and ovarian CA |
| What effect does HTN have on Organs? | Heart disease, Renal Insufficiency, CNS Dysfunction, Edema, Impaired Vision, Impaired Mobility, Vascular Occlusion |
| What is the primary source of PE's? | DVT |
| Describe Buerger's Disease | Inflammatory disease of peripheral arteries associatied with smoking. |
| Clinical Manifestations of Buerger's Disease | Pain, Rubor, Ischemia, Gangrene |
| Varicose Veins | Pooling of venous blood due to dysfunctional valves |
| Risk Factors of Varicose Veins | Standing for long periods of time, tight fitting clothes, Crossing Legs |
| Superior Vena Cava Syndrome | Progressive occlusion of SVC caused by bronchogenic CA, Lymphoma, Thrombosis, Histoplasmosis, TB, Mediastinal Fibrosis, Cystic Fibrosis, or Benign Tumors |
| LDH | Low Density Lipoprotein; increase in LDL is associated with atherosclerosis |
| HDL | High Density Lipoprotein; Increased in HDL is good. Carries cholesterol to liver for elimination; is protective against atherosclerosis. |
| Myocardial Ischemia | Decreased blood flow from atherosclerosis; cells maintain viability for 20 min; EKG changes are possible after 30-60 sec of ischemia |
| Myocardial Infarction | Irreversible cell death due to lack of O2 |
| Stable Angina | Angina Perctoris; transient Chest pain caused by chronic coronary obstruction; Usually follows activity or stress; Can be relieved by nitrates |
| Prinzmetal Angina | Occurs unpredictably and almost exclusively at rest; Associated with vasospasm of coronary artery without the presence of Atherosclerosis. |
| Labs seen in MI | Elevated Troponin (most specific to MI); Elevated CKMB, Elevated LDH; Draw labs over 18-24 hours. |
| Left Heart Failure (SYSTOLIC) Characteristics | decreased contractility/EF, Ventricular dilation resulting from increased EDV; LV hypertrophy |
| Left Heart Failure (DIASTOLIC)Characteristics | Congestive Symptoms; Pulmonary Congestion smaller ventricular size due to hypertrophy; Poor Diastolic Filling |
| Right Heart Failure Characteristics | Inability of R heart to pump blood to lungs; JVD; Edema; Can be caused by LHF. |
| Aortic Stenosis | Narrowing of aortic valve; leads to decreaed CO, LV hypertrophy,Left heart failure |
| Mitral Stenosis | Marrowing Of Mitral Valve; Atrial Hypertrophy; Decreased CO caused by less blood getting to LV; Can Lead to Pul HTN and RHF; Diastolic Murmur |
| Aortic Regurgitation | After Systole blood flows back from aorta to LV; Increased SBP and widening pulse pressure; Leads to LHF becuase of ventricular dilation |
| Mitral Regurgitation | Flow of Blood from LV to LA during Systole; loud pansystolic murmur; leads to HF; Decrease CO |
| Renal Stone Composition | Ca+/Phosphate: 70-80%; Struvite: 15%; Uric Acid: 7%; Cystine: < 1% |
| Risk factors for developing Renal Stones | Sedintary Lifestyle; decreased H2O intake; geographic location |
| What part of the urinary tract are obstructed by renal stones? | Upper Urinary Tract |
| Pylonephritis | Infection of the Upper urinary Tract(ureters, renal pelvis, interstitium); caused by urinary obstruction or reflux from bladder |
| Cystitis | Infection of the bladder; most common UTI |
| Significance of Creatinine | Molecule that is normally excreted by glomerular filtration; Elevated Cr = Kidney disease |
| Prerenal Kidney Injury | Most common cause of Acute kidney injury; hypoperfusion, renal artery stenosis |
| Intrarenal Kidne Injury | Acute Tubular Necrosis; Glomerulopathies; Malignant HTN; Renal Artery/Vein occlusion; bilatera acute pyelonephritis |
| Post Renal Kidney Disease | Obstructive Uropaty; Ureteral Destruction; Bladder neck obstruction (ex. BPH); Neurogenic Bladder |
Created by:
SRNA84
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