- Plasma
- FFP
- Indiciation:
- DIC
- Warfarin ↑
- Bleeding with ↑ PT/PTT
- Heparin antidote: Protamine
- RBC Transfusion
- Imagine patient has blood type O and needs some PRBCs (packed RBCs); what blood type donor can he get RBCs from
- Blood type O ONLY since has Ab to both A and B
- When do we transfuse?
- Impossible give rules of thumb; need use clinical judgement; but what are guidelines?
- ie. Hb level at which want to start: <70
- Symptomatic? (particuarly evidence of myocardial ischemia?)
- Anemic, evidence of ischemia
- NEVER transfuse someone who's hemoglobin is over 100;
- UNLESS patient actively bleeding (may not even wait until Hb level comes back; if someone has massive bleed, Hb concentration may not drop immediately)
- VTE
- Triad associated with predispposition to clotting: VIRCHOW'S TRIAD
- Stasis
- Hypercoagulability
- Endothelial injury
- ↑ coagulable states
- Modern name is "Thrombophilia"
- Usually think of in two groups:
- Inherited
- ↓ Protein C/S/AT III
- Factor V Leiden
- Prothrombin 21210 variant
- Acquired
- Which underlying cause of hypercoagulability would be the best first ddx for being in a hypercoagulable state?
- Estrogen
- BCP (birth control pill)
- HRT
- Pregnancy
- Tamoxifen
- Nephrotic syndrome
- Would do so because you may lose antithrombin III in urine and as a result can get venous thrombosis
- For some reason particularly prone to losing AT III
- PRV (Polycythemia Ruba Vera), ET (essential thrombocytosis) (myeloproliferative disorders)
- polycythemia ve1ra a myeloproliferative disorder of unknown etiology, characterized by abnormal proliferation of all hematopoietic bone marrow elements and an absolute increase in red cell mass and total blood volume. The skin of the face is often ruddy and swollen, and ecchymoses are common. Most patients have splenomegaly, leukocytosis, and thrombocythemia. Hematopoiesis is also reactive in extramedullary sites (liver and spleen), and in time myelofibrosis occurs. Called also erythremia, p. rubra or p. rubra vera, myelopathic or splenomegalic p., and Osler's, Osler-Vaquez, Vaquez', or Vaquez-Osler disease. Cf. secondary p.
- Site: calf --> thigh --> PE (one-third)--> fatal (one-third)
- Diagnosis
- DVT --> Doppler U/S
- PE -->
- For both can do D-Dimer
- How treat VTE?
- Initially: have to get heparin
- 2 kinds of heparin
- UFH
- Give iv, subcu for prevention; NEED to monitor!
- LMWH
- Almost always give subcu; usually don't need to monitor
- Warfarin - follow up with, overlap for a couple of days after INR is therapeutic (2-3) for a couple days and can start heparin and continue warfarin for anywhere from 3 months to LIFE! (risk factors for heart failure and breast cancer will NEVER go away)
- Leukemia
| L | Acute | Chronic |
| M | AML | CML (prv, et, IDIOPATHIC, MF) |
- Urology
- UTI
- Non-complicated
- Asymptomatic bacteremia
- Cystitis
- P.N.
- Porstatitis
- Complicated
- Instrumentation/catheter
- Immunocompromised
- DM
- Bacteria
- E-Coli
- Gram +v
- Staph saprophyticus
- Enterococcus
- Other gram -v rods (e.g. Kliebsiella)
- Note staph aurea, anaerobes, viruses, DO NOT GET INTO URINE
- 6 different antibiotic categories that can be used
- Septra / Bactrum (TMP-SMX)
- High dose septra also treatment of choice for pneumocystitis pneumonia
- Fluoroquinolones
- Nitrofuratoine (almost only use for uncmplicated UTI)
- Cephalosporins (if senstiive)
- Penicillin (amox-clav)
- Aminoglycosides
- Stones
- 4 Compositions of kidney stones
- Calcium - Oxalate or Phosphate
- Uric acid (forms in urine where pH is fairly low)
- Strubite
- Who gets them?
- People who are chronically or currenlty infected (UTI)
- pH ↓
- Risk factors for calcium stones
- Increased serum calcium leading to increased urine calcium
- Eg. Primary hyperparathyroidism causes breakdown of bone
- Hypercalciurea without hypercalcemia
- ↓ urine volume (not necessarily from being frankly dehydrated but may just drink very little water or make little urine)
- Hyperoxalemuria
- Hyperuricosuria
- Uric acid stones form when urie ph is acidic; having too much uric acid in urine means get precipated uric acid then the calcium stone forms
- Hypocitrauria
- Somebody comes in with flank pain, blood in urine, looks terrible, what is usual way nowaawdays that we find imaging evidence of kidney stones (usual way 10 15 years ago was (not U/S since doesn't show you ureters) Intravenous pyelogram (or IVP) but need lots of dye and it takes lots of time
- Preferred test nowadays is a non-contrast spiral CT
- How treat these people?
- (what going to do with patient when writhing in pain in emergency room?)
- Analgesia
- Usually give some kind of hydration (IV or PO fluids)
- Anti-emetic therapy
- Flowmax
- Alpha-1 adrenergic antagonist; used to relax the urethral sphincter; generic name is tamsulosin (an alpha blocker); dilates the ureter enough that a stone may pass
- Patients settle fairly quickly and may be discharged home
- When do you admit someone to hospital though?
- Admit if:
- Solitary kidney
- Fever etc. (look septic, leukocytosis, may have infection above the stone)
- Pain ++ (purely for reasons then of pain control)
- Nausea/Vomiting (can't therefore tolerate oral analgesia)
- Often the outcome of bringing them in is that you put in a stent
- How put it in?
- Do cystoscopy; gets cystoscope into the bladder, passes a thin tube into ureteral orifice and into renal pelvis and then suck out necessary factors
- Shockwave lithotripsy (SWL) + uteroscopy
- Preventing kidney stones
- Most important thing for them to increase (think about risk factors) is WATER INTAKE!
- Decrease oxalate, ↓sodium cause that will ↓calcium excretion
- What happens is that when have a low salt diet, you tend to be sodium avid in the kidney, so will reabsorb sodium in the kidney
- ↓ animal protein (will ↓ uric acid generated)
- NOT taking dairy and calcium actually increases kidney stone incidence SO WE DO NOT RESTRICT CALCIUM INTAKE IN THESE PATIENTS;
- Occasionally need use drugs, most common hydrochlorothiazide, increases urinary calcium excretion
- What tell them in order decrease oxalate?
- Hand them long list and have access to a dietition
- Drugs
- HCT
- Allopurinol
- Hematuria
- A little bit like jaundice
- Principle dividing lines:
- Nephrologic
- Red cell casts
- Heavy proteinuria
- Urologic
- WBCs
- Symptoms
- Pain
- Frequency
- Urgency
- Initiation or End
- Urologic Causes
- Trauma
- Infeciton
- Stone
- Cancer
- BPH
- Arteriovenous malformations
- Bleeding tendencies (Always want to rule out)
- To examine:
- Upper: U/S (CT)
- Lower --> Cystocopy
- C+S (culture and sensitivity of the urine)
- Cystoscopy
- Prostate
- Obstructive
- Hesitancy
- ↓ Stream
- 2X voiding
- Post void dribbling
- Feel incomplete emptying
- Irritative
- Frequency
- Urgency
- Urge incontinence (need to go so badly that you lose control)
- (worst kind of frequency; what drives them absolutely insane?) NOCTURIA! (hard to get restful sleep)
- Why get irritative symptoms? (classic is cystitis, inflammation of the bladder causing it to become twitchy; why these patients get this?)
- Bladder has hypertrophied (just like LVH in patient with aortic stenosis) so get terrible combination of obstructive and irriating symptoms
- Is there a direct connection between BPH and prostate cancer? NO!
- There really isn't a direct connection; bad BPH DOES NOT necessarily predispose you to prostate cancer
- NB: hypertrophy leads to thickened wall and you distend it a little and it wants to empty so they can't tolerate filling up the bladder to normal amounts
- NB: don't get dysuria; if you had cystitis, dysuria would be a mildly irritative symptom
- How Treat?
- Medical
- Alpha blockers
- Specific
- (specific bladder neck alpha antagonist): tamseclosin
- Alfuzosin
- Non-specific
- Doxazasin (also a BP med)
- 5-alpha Reductase Inhibitors
- Finasteride / Dutasteride
- Surgical
- TURP
- Transurethral resection of the prostate
- Less invasive treatments
- Microwave
- Laser
- Cryotherapy (is it laser cryotherapy or two separate categories?)
- High intensity focused U/S
- Prostate Cancer
- Risk factors
- Age
- Male
- Race (African background)
- FHx
- ↑ fat diet
- Screening (really supposed to do both)
- DRE
- PSA
- Anything you can do with PSA to make it more useful, better interpreted?
- Traditionally: greater than 4, worry about Prostate Cancer
- Multiple ones: PSA velocity (idea is that you see how somebody's PSA rises and if it rises more than a certain amount per year then not characteristic of a benign condition)
- What other than prostate
- BPH itself
- Prostatitis
- Any manipulation fo the prostate, eg.
- Cystoscopy
- Prostate biopsy
- Age norms
- Free: Total ↓(prostate cancer gives you a low fraction of PSA that is unbound)
- TRUS (transrectal U/S) guided biopsy
- Remember stage migration as it relates to prostate cancer
- From a practical view, Prostate CA in two categories:
- Localized (means potentially curable by local means; what are these options?)
- Brachytherapy (implanting radioactive seeds through the perineum into the prostate)
- Watchful waiting
- R.P. (Radical Prostatectomy)
- Conventional radiation therapy (XRT)
- Cryotherapy
- High Intensity focused U/S
- Advanced: for large, localized tumors that have spread beyond the local stage; essence of treatment is: HORMONAL THERAPY
- Castration (or bilateral orchidectomy)
- LHRH analogues (+) (implant in intramuscular depot and they constantly send out LH until cancels out pituitary secretion)
- + anti-androgen
- Combined Androgen Blockade (uses LHRH analogues AND anti-androgens
Marat's Notes
(apologies for the formatting but this is the best I could get it - ali)
Hematology
Markers for
Decrease in Hb
Anemia
Classify anemia:
- MCV
- ↓ MCV
- Causes:
- Fe def
- Causes
- Poor absorption, poor diet
- Menstruating women
- GI lesions
- Tests:
- BM biopsy – Gold standard (stain for Fe)
- Fe/TIBC (total Fe binding capacity)
- Iron saturation
- Anemia of chronic disease (ACD)
- E.g. (Sarcadosis, Malignancy Rheumatologic disease)
- Fe not available for RBC production
- Fe stores normal
- All 3 affect Hb → that’s why the cells are small
- ↑MCV
- Megaloblastic
- ↓vit B12
- Causes:
- Poor diet
- ↓ absorption
- Pernicious anemia
- Terminal ileum disease (Chrons)
- EtOH
- Liver disease
- ↓ T4
- Myelodysplasia
- ↑ retics
- N MCV
- Most of the above can be normocytic
- BM disease
Hemolysis
Mechanisms of hemolysis:
- exterior
- immune
- autoimmune hemolytic anemia (AIHA)
- warm (thermal amplitude of antibodies, cause hemolysis at warmer temperatures)
- SLE, CLL
- HIT (heparin induced thrombocytopenia)
- non-immune
- MAHA (macroangiopathic hemolytic anemia)
- TTP (thrombotic thrombocytopenic purpura)
- RBCs sliced up when they go past the clot
- HUS (hemolytic uremic syndrome)
- DIC
- Malignant hypertension
How to recognize hemolysis?
- tests
- Blood film
- Shistocytic (fragmented) cells
- Spherocytes
- Coombs tests (detects RBCs coated with antibodies)
- ↓ haptoglobin (scavenges Hb → binds to Hb → removed together)
- ↑ retics
- ↑ LDH (high inside RBCs)
- ↑ Bilirubin (b/c of ↑ release of heme)
Increase in Hb
- ↓ plasma volume
- Renal cell carcinoma
- Polycythemia ruba vera (PRB)
- Blood doping
- ↓ PO2
↑ bleeding
- Platelets
- ↓ number
- ↓ production
- ↑ destruction
- Immune
- ITP (idiopathic thrombocytopenic purpura)
- +/- SLE/CLL
- HIT
- HIV
- Sequestration
- ↑ spleen
- Inflammatory
- Sarcoid (non-caseating granulomas), SLE
- ↓ function
- ASA et al. (other NSAIDS, Plavix (clopidegrel))
- Uremic syndrome
- coagulation
- Inherited
- F8 (hemophilia A – more common)
- F9 (hemophilia B)
- Acquired
- ↓ Vit K
- Causes:
- Nutrition
- Mal-absorption
- Antibiotics (b/c vit K comes form bacteria)
- warfarin
- Massive transfusion
- Liver failure
- DIC
Platelet transfusion
- N platelet count (150-400 x 10^9/L)
- Counts:
- < 10 → transfuse
- Unless ITP (b/c platelets will get destroyed right away)
- < 50 → if going for surgery then transfuse
- < 100 → if there are CNS issues (e.g. brain surgery)
- Any platelet count BUT there is active bleeding → transfuse
Plasma
- FFP
- Indications:
- DIC
- ↑ warfarin
- Active bleeding with ↑ PT/PTT
- N.B. – if pt on heparin, plasma will NOT help
- Need to use antidote – protamine
RBC transfusion
- pt is type O + needs RBCs
- can only get O
- type O is a universal DONOR, but if need blood themselves → need O-type
- when to transfuse:
- [Hb] < 70
- Symptomatic patients
- bleeding
Venous thrombo-embolism (VTE)
- Virchow’s triad
- Stasis
- Endothelial injury
- ↑ coagulation state
- Inherited
- ↓ Protein C/S/AT3 (not common)
- F5 Leiden (F5 resistant to Protein C)
- PT 20210
- Acquired
- Myeloproliferative diseases
- PRV (polycythemia ruba vera - Primary polycythemia, often called polycythemia vera (PCV), polycythemia rubra vera (PRV), or erythremia, occurs when excess red blood cells are produced as a result of an abnormality of the bone marrow.)
- ET (essential thrombosis)
- Site
- Calf → thigh → 1/3 PE → 1/3 fatal
- Diagnosis
- DVT → Doppler U/S
- PE → V/scan, CT angio
- D-dimers
- Treatment of VTE
- Heparin
- LMWH
- S.c.
- No monitoring, can Tx at home
- Warfarin – target INR 2-3
Hematological malignancies
| | Acute | Chronic |
| Lymphoid | ALL | CLL |
| Myeloid | AML | CML (PRV, ET, idiopath, mf) |
Lymphoma
Multiple myeloma
Urology
UTI
- Complicated
- Pregnant
- Instrumentation, catheter
- ↓ immunity
- DM
- Bacteria
- E.Coli
- Gram +
- Staph sap (not S.aureus)
- Enterococcus
- Other Gram –ive rods
- Note (no viruses)
- Antibiotics
- SeptraTM (TMP Smx) – most commonly used in UTIs
- Also used in pneumocystis pneumonia
- FQ (fluroquinilones) → Cipro
- Nitrofurantoin
- Cephalosporins
- Amox-Clavulin
- A/G
Kidney stones
- Types:
- Ca-oxalate (Ca-PO4)
- Uric acid (↓pH)
- Struvite (UTI) ↑pH
- Cystine
- Risk factors for Ca stones:
- ↑ serum Ca → ↑ urine Ca (primary hyperparathyroidism)
- Hypercalciuria
- ↓ urine volume
- Hyperoxaluria
- Hyperuricosuria (↑ uric acid in urine → forms precipitate → Ca stone forms on top)
- Hypocitrauria (↓ citrate in urine)
- Renal/ureteral colic:
- tests:
- CT (non-contrast spiral)
- N.B. Intravenous pyelogram was done in old days b/f CT
- Tx:
- Analgesia
- i.v. + p.o fluids
- Anti-emetic
- Flowmax (tamsulosin, a-blocker, relaxes sphincter)
- Admit to hospital if:
- Solitary kidney (the other kidney is obstructed)
- Fever, leukocytosis, etc → worried of infection
- Pain +++ (for pain control)
- Nausea/vomiting (can’t tolerate oral analgesia)
- Eventual Tx:
- Stent
- Shock wave litotripsy (SWL) +/- ureteroscopy
- Prevention of kidney stones
- ↑ fluids (water)
- Diet changes
- ↓ oxalate
- ↓ Na → ↓ Ca excretion
- Orange or lemon juice → ↑ citrate
- ↓ animal protein (↓ uric acid)
- Normal Ca diet
- Take dairy → removes oxalate from gut
- Drugs
- Hydrochlorothiazide
- Allopurinol to decrease uric acid
Hematuria:
- Urologic
- At initiation (problem in urethra) or at end of voiding (bladder trigone)
Urologic Causes
- Kidney, ureter, bladder
- Trauma
- Infection
- Stone
- Cancer (most concerned about)
- Also:
- BPH (in older men)
- AVM (arterial venous malformations)
- R/o bleeding tendency
- Work up:
- upper tract → U/S (CT)
- Lower tract → Cystoscopy
- C/S
- cytology
Prostate
BPH
- Symptoms:
- obstructive
- hesitancy
- ↓ stream
- 2x voiding
- Post void dribble
- Incomplete emptying
- Irritative
- Frequency
- Urgency
- Urge incontinence
- Nocturia
- Treatment
- Medical
- A-blockers
- Specific
- Tamsulosin (Flowmax)
- Alfuzosin
- Surgical
- TURP (transurethral resection of prostate)
- Less invasive
- Microwave, high intensity U/S
Prostate Cancer
- Risk factors
- Age
- Male
- Race (African Americans)
- ↑ fat diet
- PSA
- PCA velocity (observe how it changes with time)
- Age norms
- Free:Total ↓
- Diagnosis
- TRUS (Trans-rectal U/S guided)
- Stage migration (most cancer was advanced 20years ago, no mostly localized)
- Types
- Localized
- Watchful waiting
- Brachy-therapy
- Radical prostatectomy
- Radiation therapy
- New stuff (Cryotherapy, high energy U/S)
- Advanced
- Hormonal therapy
- Castration (bilateral orchidectomy)
- LHRH analogues (i.m. depo → bombard pituitary → stops body’s LHRH production → stops T production)
- +/- anti-androgen
- CAB (combined androgen blockade)