FINAL EXAM Study Guide Version Part 1 Flashcards
Understand the ABG’s and how to decide if a patient is in resp acidosis or resp alkalosis, Metabolic acidosis, or metabolic alkalosis.
FUNCTION OF POTASSIUM
- K+ necessary for normal cardiac rhythms.
- K+ necessary for skeletal and smooth muscle contraction.
- K+ helps make glycogen deposit in the liver.
- Yum Yum Potassium :D
- Administration: NO IV PUSH, Oral and IV.
FUNCTION OF SODIUM
- It’s the main regulator of ECF volume! (Hence, more sodium you balloon up)
- Administration: Hypertonic fluids
FUNCTION OF CALCIUM
Low calcium: Tetany, Chvostek + sign, Trousseau +
Ca++ works as an enzyme co-factor for clotting and hormone secretion. Stored in parathyroid glands.
- Ca++ maintains plasma membrane stability-particularly in the cardiac cell nerve receptors.
- Ca++ aids in the transmission of nerve impulses and contraction of muscles.
- Administration:
- Acute situations give Calcium Gluconate IV PUSH slow
- Non-Acute give Calcium PO
CORRECTED CALCIUM FORMULA!
measured Ca(mg/dL) + 0.8(4.0 - serum albumin g/dL) = Corrected calcium (mg/dL)
Example:
Pt’s serum calcium level is reported as 7.5 mg/dL and serum albumin is 2.5 g/dL.
7.5 mg/dL + 0.8(4.0-2.5 g/dL) =
7.5 mg/dL + 1.2 = 8.7 mg/dL (corrected calcium)
ANGINA
vs.
MI
Angina is a result of ischemia caused by reversible cell injury.
MI: Coronary artery occlusion with myocardial death and necrosis. WE HAVE AN ST ELEVATION OMG - every medical drama show ever….
MI INTERVENTION
- Oxygen therapy: keep 02 sat > 95%.
- Aspirin: 325 mg chewable
- Metoprolol: 5 mg IV push
- Morphine: 2-10 mg IV push
- Nitroglycerin IV titrate to pain and BP
- 12 lead ECG: monitor for S-T elevation, depression.
- Cardiac enzymes- CPK-MB, LDH, Troponin T/I,
- electrolytes, CBC.
- GET THAT PATIENT’S ASS TO A CATH LAB, or umm he’s gonna die
Cardiac markers (labs) for a patient having an MI
- Topononin I & T (Most reliable)
- CK (Creatine Kinase)
- Myoglobin
Current standard of care for a patient having an MI
Reperfuse heart via Percutaneous Coronary Intervention or PCI with/without stents.
signs and symptoms of decompensated heart failure
- SOB
- Fatigue
- DOE
- Orthopnea (Wake up cause they can’t breathe)
- Paroxysmal Nocturnal Dyspnea
- Tachycardia (Compensation of fluid load)
- Poor Activity Tolerance
- Fluid weight gain
- Edema (LE, pulm)
- Nocturia
- Skin changes (Greyish color)
- Chest pain (give nitro, check for MI)
- Cough (Can be productive, if they are foaming at the mouth, then they are drowning - Medical Emergency))
- Hepatomegaly
- Anorexia/Nausea
Medications given for heart failure management
- ACE inhibitors-1st line therapy in all stages of HF for both systolic and diastolic HF.
- Diuretics- Lasix, HCTZ
(That hydro chloro Thiazide), (watch electrolyte levels, monitor intake/output)
Given IV push (not PO)
- Inotropes- Digoxin (measure serum levels)
- B-Adrenergic Blockers- Metoprolol
- Calcium channel Blockers- Amlodipine
- Vasodilators- Imdur
- Antiarrhythmics- Amiodarone
- Blood thinners, platelet inhibitors- ASA, Plavix,
- Nitrates/ vasodilators
- s/s of digoxiticity: HTN, nausea, fatigue, U wave after T wave on ECG
- B-Adrenergic Blockers- Metoprolol (given because the faster the heart goes, the less CO so BB help slow it down to function properly)
- know the HR before giving
- Calcium channel Blockers- Amlodipine (Know heart rate)
- Vasodilators- Imdur
- Antiarrhythmics- Amiodarone (KNOW THIS)
- s/s: Turns you into a smurf (blue), pulmonary fibrosis, Liver function goes bad, hyperthyroidism leading to AFib, blindness
- Used to treat atrial fib, and ventricular fib but can also cause your a. fib
- Blood thinners, platelet inhibitors- ASA, Plavix, Coumadin (Vitamin K and FFP reserve it and you need to check INR normal 2-3)
- Nitrates/ vasodilators
- SE: low BP and headache
criteria for normal sinus rhythm
- There is a P-wave in front of every QRS. (0.06 to 0.12)
- Distance between P wave and QRS complex is the same in each complex.
- Distance between R-R waves is the same.
- Rate is between 60-100 beats per minute.
- Rate increases as metabolic demand increases with activity- ex: exercise
Ventricular Tachycardia
- Heart rate is 100-280 , Cardiac output is minimal
- Treatment: When patient is unconscious, DEFIB them or cardioversion
- first thing you do is look at them (assessment)
- Due to scar tissue from previous MI.
- no BP, no HR, nothing
Atrial Fibrillation
- Impulses stop at AV node, got atrial quiver at over 400-600 bpm.
- CAN THROW A CLOT, stroke guys :(
- Treatment: RATE vs RHYTHM control. so slow the heart (Beta blockers and CCB), and give antiarrhythmics (Amiodarone). ALso give heparin to prevent clots.
- count the R to R interval
- Can also cardiovert or ablation
- No visible P-wave
Ventricular Fibrillation (CODE BLUE)
- Defib that patient’s ass or he ain’t gonna be alive. (Defib ASAP)
- CPR, Pharm management (Amiodarone, epi, etc.)
- No Respirations or pulses
- START CPR
Indications for Coumadin therapy and the patient teaching and bleeding precautions that are associated with Coumadin therapy.
- Coumadin for them A Fib boys
- Give Coumadin for atrail fibrillation as prophylaxis to prevent clots and strokes
- Try not to hurt your self or you’ll bleed to death
- Keep vitamin K the same, so don’t chug them leafy greens
signs and symptoms of acute respiratory failure
- Sudden and life threatening deterioration of gas exchange function of the lung.
- Defined as:
- * a decrease in PaO2 to < 50 mm Hg (hypoxemia)
- * an increase in PaCO2 to > 50 mm Hg (hypercapnia)
- * an arterial pH of < 7.35 (acidemia).
- Tachypnea, dyspnea with prolonged expiratory phase - approximately 1:4.
- SpO2 less than 80%
criteria for a diagnosis of ARDS
A clinical syndrome characterized by:
- sudden and progressive pulmonary edema
- increasing bilateral infiltrates on chest x-ray
- hypoxemia that is refractory to oxygen therapy
- reduced lung compliance.
- These signs occur in the absence of left-sided heart failure
- No response to O2 therapy
cardinal signs of a patient with COPD
Characterized by 3 primary symptoms:
- Cough
- Sputum production
- Dyspnea on exertion
o Weight loss as dyspnea interferes with eating
o Energy-depleting work of breathing
o Use of accessory muscles to breathe
o Appearance of a barrel chest from fixation of the ribs in inspiratory position (hyperinflation)
- Hx of smoking
COPD Medical Management
· Smoking cessation: MUST ask patient. Most effective intervention
· Bronchodilators: MDI’s and nebulizer therapy (for acute COPD exacerbation)
o Beta adrenergic agonist agents
o Anticholinergic agents
o Methyxanthines
· Corticosteroids: inhaled and systemic (for short bursts only)
o Do NOT take continuously (S/E profile: bone loss, high Glu)
· Oxygen therapy: long-term continuous O2 therapy in LOW doses
o PaO2 of 55mmHg or less needs O2
o Any evidence of organ damage needs O2
rule of nines in estimating burn percentages on a patient
- Any burn greater than 40% TBSA will have systemic effects
Parkland formula in determining the amount of fluid replacement a burned patient will need in the first 8 hours and the next 16 hours
- Urine output above 50 an hour, BP over 80/50
- Give the fluid central Line.
goals of cancer therapies (cure, control, palliation), and what to do if a patient has an implanted radiation device that suddenly becomes explanted
- *Cure:** can the cancer be completely removed? (stage 0-1)
- *Control:** can we limit/stop the spread? (stage 2-3)
- *Palliation:** can we keep the patient comfortable? Say Goodnight Crazy (aka stage 4)
In event of dislodged implant- use long-handled forceps and place implant in lead container
3 things a nurse needs to remember when dealing with a patient with a radiation implant - in terms of protecting herself
Time: minimize time spent in close contact
Limit total time to 30 min per total 8 hour shift
Minimum 6 feet of distance when possible
Distance: maintain maximum distance possible from radiation source
Shielding: use lead shields to reduce exposure
In event of dislodged implant- use long-handled forceps and place implant in lead container
CAUTION algorithm for warning signs of cancer
C: change in bowel or bladder habits (color, hematuria #1 sign)
A: a sore that does not heal
U: unusual bleeding or discharge
T: thickening or lump in breast or elsewhere
I: indigestion or difficulty in swallowing
O: obvious change in mole or wart
N: nagging cough or hoarseness
S: sudden and unexplained weight loss
TNM staging for cancer
- *T-** the extent of the tumor
- *N-** the absence or presence and extent of lymph node metastasis.
- *M-** the absence or presence of metastasis
4 drug regimen for a patient having an anaphylactic reaction
Epinephrine 1:1,000 dilution injection
- SubQ in upper arm or thigh
Antihistamine
- Benadryl (Diphenhydramine) 25-50 mg IV push
Corticosteroid
- Solucortef or solumedrol 150 mg IV push
H2 Receptor blocker
- Pepcid, etc.
Localized Response
to Anaphylactic Reaction
- -Pruritus
- -Rhinitis
- -Rash
- -Redness
- -Fever
- -Urticaria
Systemic Response
to Anaphylactic Reaction
SYSTEMIC RESPONSE: WORSE TYPE OF REACTION- MAY BE FATAL IF NOT TREATED QUICKLY!!!
- Massive vasodilation: causes sudden drop in BP
- Increased capillary permeability
- Smooth muscle contraction: gastrointestinal and uterine spasm
- Laryngeal stridor and edema: bronchospasm
- Angioedema
CATEGORIES OF ANAPHYLACTIC REACTIONS
- *Mild-** peripheral tingling, sensation of warmth, fullness in mouth and throat, nasal congestion, peri-orbital swelling, pruritus, sneezing. Symptoms begin within 2 hours of exposure.
- *Moderate-** flushing, warmth, anxiety, itching, cough, wheezing, bronchospasm, and any or all of the above mild symptoms. Onset begins within 1 hour of exposure.
- *Severe-** abrupt onset of symptoms beginning with mild and moderate and quickly progressing to laryngeal edema, cyanosis, severe dyspnea, and hypotension. Dysphagia, vomiting, diarrhea, and seizures may also occur followed by cardiac arrest and coma.
HOW IS HIV CONTRACTED
- Sexual Contact; unprotected sex = Primary transmission
- Person receiving semen is more likely to have HIV transmitted to them
- Blood, needle sharing, drug paraphernalia = 2nd route of transmission
- Birth, in utero, breast milk
- (HIV that is undetectable , is untransmissable)
The current HAART therapy for treating HIV
4 drug regimen → Combination therapy
Dosages are fixed in combination drugs
2 NNRTI’s, Integrase inhibitor, and Protease inhibitor
Goals of drug therapy:
- Decrease the viral load
- Maintain or increase CD4+ T cell counts
- Prevent HIV related opportunistic diseases
- Delay disease progression
- Prevent HIV transmission
CLINICAL MANIFESTATIONS OF
AUTOIIMMUNE
SYSTEMIC LUPUS ERYTHEMATOSUS (SLE)
Musculoskeletal: 90% joint involvement, similar to RA but no RF and no joint destruction
Integumentary: rashes, “butterfly” rash on nose, cheeks; alopecia, sun sensitivity, mucous membrane lesions
Cardiovascular: pericarditis, ischemic heart disease
Pulmonary: pleural effusion, pneumonitis, PE
Renal: glomerulonephritis, nephrotic syndrome
Neurological: 30-75%; vasculitis leads to CVA, seizures, depression, psychiatric complications
Hematopoietic: hemolytic anemia, leukopenia, lymphopenia, thrombocytopenia, lymphadenopathy with lesions on head, scalp, neck.
CLINICAL MANIFESTATIONS OF
RHEUMATOID ARTHRITIS
- -Joint pain, redness and warmth with swollen effusions
- -Lack of joint mobility and function bilaterally
- -Joint instability, contractures
- -Deformities of the hands and feet
- -Fatigue, malaise, anorexia
- -Elevated body temperature
- -Subcutaneous nodules on joints
- -Limited ROM, paresthesias of hands/feet
- -Morning stiffness and crepitus
- -Pericarditis, Leukopenia
- -Splenomegaly, Enlarged lymph nodes
- -Anemia
- -Lymph node enlargement
- -Peripheral Neuropathy
- -Raynaud’s phenomenon- cold and stress induced vasospasm of the hands and feet giving them a cyanotic (bluish) appearance.
- -Ulnar drift
- -Boutonniere deformity
- -Hallux Valgus
- -Swan-neck deformity
LAB DIAGNOSTIC OF SLE
- ESR: blood test to determine rate at which RBC’s reside to the bottom of the test tube over the course of an hour. Faster rate is indicative of infection.Notice I said infection and not just lupus, this test does not 100 percent verify diagnosis of lupus but elevated ESR is present in the case of lupus.
- ANA: test for presence of antibodies (+)
- Urinalysis: to detect blood or proteins in the urine
LAB WORK FOR DIAGNOSIS OF RA
- Serum rheumatoid factor is present in 80 %
- Elevated erythrocyte sedimentation rate (ESR) indicates inflammation
- C-reactive protein is positive (CRP) indicates inflammation
- RBC’s decreased
- C4 complement is decreased
- Serum Antinuclear antibody (ANA) is positive
MEDICAL and NURSING
management of SLE
MEDICAL MANAGEMENT
- Corticosteroids are the single most important medication used for treatment.
- Prednisone: Used in low oral doses for remissions and in high doses (IV if needed) for exacerbations. Must NEVER be stopped abruptly!! Always a tapered reduction of dose.
- Anti-malarial medications, alkylating agents and purine analogs are used for serious forms that do not respond to conservative therapies.
NURSING MANAGEMENT
- Decreasing fatigue
- Promoting restorative sleep
- Providing protection for impaired skin integrity
- Sun and ultraviolet light exposure can increase disease activity or cause exacerbation-
- Facilitating self-care
- Improving body-image and coping
- Monitoring and managing potential complications- cardiac and renal involvement
MEDICAL and NURSING
management of RA
MEDICAL MANAGEMENT
- -NSAIDs, anti-Rheumatics, corticosteroids, immunosuppressants
- -NSAIDs, splints, thermal heat, relaxation
- -Exercise programs and muscle strengthening
- -Adaptive devices
- -Provide and reinforce patient teaching
- -Emphasize therapeutic regimen and lifestyle
NURSING MANAGEMENT
- -Achieve adequate pain control
- -Decrease fatigue
- -Promote restorative sleep
- -Increase mobility
- -Facilitate and encourage self-care
- -Improve body-image and coping
- -Monitor and manage potential complications
- -Promote home and community-based care/ resources
- -Balancing periods of activity with rest
- -Exercise to maintain joint function and mobility
- -Patient support related to chronic illness
- -Assistive devices for joint protection
- -Support groups and other information
Difference between DM type 1 and DM type 2
Type 1
- No insulin secretion at all / beta cells destroyed
- MUST be given insulin
- Signs: 3 P’s
- Polyuria
- Polyphagia
- Polydipsia
- Weight loss
- Fatigue
Type 2
- Some insulin secretion but not enough / receptors not sensitive to insulin. Happens over time.
- Initially treat with diet/exercise but if not controlled use insulin as well like metformin
- Don’t get v high BG levels around 800-900 like type 1 does
-
Signs:
- Fatigue
- Poor wound healing
- Recurrent infections (ex: yeast)
- Vision changes
- Paresthesia
CLINICAL MANIFESTATIONS OF
HYPOGLYCEMIA
Skin and muscle: profuse sweating, tremors,
Cardiovascular: tachycardia, palpitations
Head region: numbness of lips and tongue, slurred speech, double vision
Neuro: nervousness, inability to concentrate, headache, confusion, memory lapses, irrational or combative behavior, drowsiness
Stomach: hunger!
Severe hypoglycemia may cause disorientation, seizures, and loss of consciousness, DEATH
CLINICAL MANIFESTATIONS OF
HYPERGLYCEMIA
Cardiovascular: hypotension, tachycardia
Head region: profound dehydration so really thirsty, blurred vision
Neuro: headache, confusion, memory lapses, irrational or combative behavior, drowsiness
MICROVASCULAR and MACROVASCULAR complications of patients with DM
Macro-vascular changes
- Heart (CAD), brain (cerebrovascular disease), peripheral vascular system (accelerated atherosclerosis), neuropathies (paresthesia, foot ulcers)
Micro-Vascular changes
- Eyes (retinopathy), kidneys (nephropathy so monitor kidney)
DIABETIC KETOACIDOSIS (DKA)
- Hyperglycemia of Type 1
- Breaking down fat for energy causes release of ketones which are acidic
- Severe dehydration, metabolic acidosis, fruity breath, hyperventilation with Kussmaul respirations, abdominal pain, n/v, sudden weight loss, polyuria, polydipsia
- Tx: 1st thing to do = FLUID REPLACEMENT 0.9% NS (if pollute, want to dilute), 2nd O2 because metabolic acidosis, 3rd regular insulin IV push
HYPERGLYCEMIC HYPEROSMOLAR
NONKETOTIC SYNDROME (HHNS)
- Hyperglycemia of Type 2
- More serious than DKA
- No ketones in urine
- Hypotension (bc dehydrated), tachycardia, altered LOC
- Tx: rehydration, insulin administration
Signs and Symptoms of Hypothyroidism
- TSH > 4.0
- Myxedema (non-pitting edema), confusion, can progress to stupor, coma, death
- Slow metabolism manifestations
- Fatigue, hair, skin, nail dryness, paresthesia, hypothermia, bradycardia, weight gain, slow speech
Signs and Symptoms of Hyperthyroidism
- TSH < 1.0
- Poor heat tolerance, tachycardia, exophthalmos (bulging eyes), increased appetite but weight loss, high BP
- Increases chance for A.Fib.
ACUTE RENAL FAILURE
PRERENAL
PRERENAL: Azotemia caused by hypo-perfusion of the kidney. Sudden severe drop in BP (shock) or interruption of blood flow to the kidneys from severe injury or illness.
VOLUME DEPLETION AS A RESULT OF:
- Hemorrhage
- Renal losses: diuretics, osmotic diuresis
- GI losses: vomiting, diarrhea, nasogastric suctioning
IMPAIRED CARDIAC FUNCTION DUE TO:
- Myocardial infarction, heart failure, dysrhythmias, shock
VASODILATION RESULTING FROM:
- Sepsis, anaphylaxis, vasodilatory medications- antihypertensives
ACUTE RENAL FAILURE
INTRARENAL
INTRARENAL: The renal parenchyma or nephron is damaged. Damage to renal tubules or glomeruli occurs. Direct damage to the kidneys by inflammation, toxins, drugs, infection, or reduced blood supply.
PROLONGED RENAL ISCHEMIA:
- Most common cause is ATN (acute tubular necrosis)
- Pigment nephropathy (breakdown of blood cells containing pigments that occlude kidney structures)
Myoglobinuria (trauma, crush injuries, burns)
Hemoglobinuria (transfusion reaction, hemolytic anemia)
Rhabdomyolysis-colored urine due to muscle breakdown
Infectious processes: Pyelonephritis, Glomerulonephritis
Nephrotoxic agents such as:
- Aminoglycoside antibiotics- Gentamicin, Tobramycin, Vancomycin
- Radiopaque contrast agents used in CAT scans and Angiograms
- Heavy metals- lead, mercury
- Arsenic poisoning
- NSAID’s, ACE inhibitors
ACUTE RENAL FAILURE
POSTRENAL
POSTRENAL: urine outflow is obstructed. Sudden obstruction of urine flow due to enlarged prostate, kidney stones, bladder tumor, or injury.
URINARY TRACT OBSTRUCTION:
- Calculi- renal stones
- Tumors
- Benign Prostatic Hyperplasia (BPH)
- Flomax! or TURF (transurethral resection of the prostate gland)
- Urethral strictures
- Obstructive blood clots
Most common cause of chronic renal failure
HYPERTENSION & DM
- HTN and DM
- Think about it, HTN causes perfusion issues to kidneys, and diabetes messes up pretty much everything
TWO TYPES OF DIALYSIS
PERITONEAL
Peritoneal: uses a peritoneal membrane
- Can be done by patient independently at home. Patient can maintain a fairly normal lifestyle. PD can be done at night while sleeping or the patient can do cycles during the day (about every 4 hours)
- 2 types: automated and continuous
- Catheter is surgically implanted in abdomen
- Peritoneal membrane is used as semipermeable membrane
- 2L of dextrose: 1.5%, 2.5%, or 4.5% are infused into the abdominal cavity. Called fill cycle à dwells in cavity. Called dwell cycle à fluid is then drained and weighed to make the same amount is drained as was filled. Called drain cycle à abdomen filled with dialysate
- Complications: peritonitis, infection caused by staph aureus or staph epidermidis
TWO TYPES OF DIALYSIS
HEMODIALYSIS
Hemodialysis: uses cellulose or synthetic material as semipermeable membrane
- Done at a center or in hospital and is done three days a week and takes about 4 hours for each session
- Two 14-16 gauge needles are inserted into fistula or graft for access à attached via tubing to dialysis lines using sterile technique à one needle pulls blood into dialyzer machine and other is to return clean blood to patients
- A thrill can be felt by palpating the anastomosis and a bruit can be heard with a stethoscope
- Strict following of dietary restrictions necessary for optimal management
Criteria for a patient to receive a renal transplant
- Be a blood type match
- BUT, ESRD (End stage renal disease), When that good old GFR is less than 15 (Also known as stage 5 Kidney Failure)
SIGNS of rejection do you want a renal transplant patient to know and monitor themselves for after they go home
SIGNS OF REJECTION
- Elevated BUN and creatinine
- Fever
- Weight gain
- Decreased urine output-oliguria
- Increased blood pressure
- Tenderness or swelling over the transplanted kidney
- Elevated white blood cell count
- Rejection is confirmed by renal biopsy
SO, what can a patient monitor themself for?
- DECREASED URINE!!
- Fever, weight gain, tenderness over kidney. Basically, any thing you can detect without fancy machines. Hence my rule (Love’s) , if you feel like crap, you probably are in some kind of crap. So go get checked out.
Long-term effects of corticosteroids
- Clouding of the lens in one or both eyes (cataracts)
- High blood sugar, which can trigger or worsen diabetes
- Increased risk of infections
- Thinning bones (osteoporosis) and fractures
- Suppressed adrenal gland hormone production
- Thin skin, bruising and slower wound healing
- (MAKE SURE, always wean off steroid use or you will have the addisionian crisis)
ADDISONIAN CRISIS
- extreme weakness
- mental confusion
- dizziness
- nausea or abdominal pain
- vomiting
- fever
- a sudden pain in the lower back or legs
- a loss of appetite
- extremely low blood pressure
- chills
- skin rashes
- sweating
- a high heart rate
- loss of consciousness
Clinical manifestations of dehydration?
In other words, what would you expect to see in their vital signs?
- Drink some water - obviously
- So simple, less water in the system. So less pee you piss out, and low bp cause there’s barely any water :(
- Hypotension
- Decreased Urine Output, That sewer water colored pee (Dark urine)
- Dizziness
- Tachycardia
- Skin turgor goes down
- Strict Vital’s wise: BP down, Heart rate up, Respirations up
Other organ systems may be affected by medications that are nephrotoxic
Ototoxic drugs also nephrotoxic
Lasix/loop diuretics, aminoglycosides (vancomycin, gentamycin)
Clinical signs and symptoms of a patient with liver failure and what lab work would verify the diagnosis?
- Ummm the patient looks like a simpsons character (Jaundice, check Sclera of the eyes first, and then skin manifestations)
- Bilirubin Elevation
- Albumin Down
- Liver function tests go up (ALT up, AST up)
- Here’s a cool way I remember it :)
- ALcoholics Test (A.L.T)
- AlcoholicS Test (A.S.T)
- Portal hypertension, ascites, and esophageal varices
- Hepatic encephalopathy, or Coma (Happens cause of ammonia)
Differences between ulcerative colitis and Crohn’s disease in terms of what part of the bowel is affected
Reason for a patient to develop hepatic encephalopathy and what is the treatment?
- If the patient has liver failure / cirrhosis
- IV glucose (Prevent protein catabolism)
- Lactulose (Its a pooping med lol. But you don’t use it for the poops, but to remove ammonia :D) don’t stop using it, just cause your patient shitted 5 times today, look for LOC changes.
Ronson’s criteria for a patient with pancreatitis
IF YOU HAVE THESE, boy I hope you live. Greater than 60% chance to die.
- Age > 55 years
- WBC > 16,000/Ul
- Blood glucose > 200 mg/dl
- Serum LDH > 350 IU/L
- AST > 250 IU/L
- Hct dropping > 10 %
- BUN increase 5 mg/dl, U/O decreasing
- Pa02 < 60 mm Hg
- Serum Ca+ < 8 mg/dl
The treatment for a patient with Helicobacter pylori induced ulcers
- Give that yum yum pepto
- 1 PPI, 2 Antibiotics, and……. PEPTOOOOOOOO
Nephrolithiasis and be able to discuss ways to treat these stones
Darn Kidney stones …. (Renal Calculi)
Treatments:
IV Fluids, plus meds (Flomax and Hytrin)
Surgery
- Nephrolithotomy
- Pyelolithotomy
- Ureterolithotomy
- Cystotomy
Pyelonephritis and how is it treated
Inflammation of renal parenchyma and collecting system
Treatment:
Uncomplicated: Treat with antibiotics 3 days
Complicated: 7 to 10 days
Glomerulonephritis and how is it treated
Inflammation of the kidney (Specifically the glomerulus)
Treatment: DEPENDS ON CAUSE (and treat underlying cause)
Always remember to treat cause, so that will help you with Tx.
Strep (Antibiotics)
Lupus (Steroids)
Goodpasture (Plasmapheresis)
