Deck 3 Flashcards
What antibiotics cover anaerobes
Clindamycin Metronidazole Moxifloxacin Amox-clav Pip-tazo Ertapenem
What antibiotics cover ESCAPPM bacteria
Cipro Gentamicin Ceftazadime Cefepime Meropenem
What are the ESCAPPM organisms?
Enterobacter Serratia Citrobacter Aeromonas Proteus Providencia Morganella
What antibiotics cover pseudomonas?>
Cipro Gentamicin Ceftazadime Cefepime Meropenem Pip-tazo
What antibiotics cover E. coli, klebsiella and proteus?
Cipro Gentamicin Moxifloxacin Ceftriaxone Ceftazidime Cefepime Pip tazo Amixicillin-->ecoli and klebsiella only Amox clav--> ecoli and klebsiella only Meropenem Ertapenem
What antibiotics cover strep?
Penicillin Amoxicillin Cephazolin Clindamycin Vanco, linezolid Cipro Moxifloxacin Cefuroxime Ceftriaxone Cefepime Amox clav Pip tazo Meropenem
Which antibiotics cover MSSA?
Cephazolin Clindamycin Rifampin Vancomycin Linezolid Cipro Cefepime Amox clav Piptazo Meropenem
Which antibiotics cover MRSA
Clindamycin Rifampicin Vancomycin Linezolid Daptomycin
What is typical angina
All three of–
- Substernal chest discomfort or heaviness
- Provoked by exertion or emotional stress
- Relieved by rest or nitro
(Atypical angina is two of the above)
(Non cardiac chest pain is none of the above)
What helps you call something “non cardiac” chest pain
None of the three features of typical angina
What are the CCS classes of angina?
I–chest pain with strenuous exercise
II–chest pain with more than two blocks flat ground or more than 1 flight of stairs
III–chest pain with 1-2 blocks flat ground or 1 flight of stairs
IV–chest pain at rest
What causes oxygen demand in the heart
HR
Contractility
Wall stress
What determines blood supply to the heart
Coronary vascular resistance
Oxygen carrying capacity
Coronary perfusion pressure
What are the 5 types of MI
- Type 1–spontaneous MI due to primary coronary event (atherosclerotic plaque rupture or erosion with acute embolic event)
- Type 2–MI secondary to ischemic imbalance (supply demand mismatch)
- Type 3–MI resulting in death when bio marker values are unavailable (sudden unexpected cardiac death before serum bio markers are collected for measurement)
- Type 4–MI related to PCI or stent thrombosis
- Type 5–MI related to CABG
What is an ACS
One of unstable angina, NSTEMI, STEMI
Define unstable angina
One of:
- Rest angina lasting more than 20 min
- New onset angina (angina CCS more than III within two months of initial presentation)
- Increasing angina (crescendo pattern–increased by at least one CCS class within two months of presentation to at least CCSIII)
Define NSTEMI
Any of the features of unstable angina with bio marker elevation (with or without ECG changes)
Define STEMI
Defined by ECG changes
What are the non modifiable cardiac risk factors
Age
Gender
Family history
What are the modifiable cardiac risk factors
Diabetes
HTN
Hyperlipidemia
Smoking
Which bio markers are the most specific in ACS?
CKMB and troponin but are typically not elevated until 4-8 hours after the injury and must be repeated at q6h initially
What are some other things other than ACS that can cause a rise in troponin
Demand ischemia–> sepsis, LVH
Myocardial ischemia–> coronary vasospasm, stroke
Direct myocardial damage–> cardiac contusion, chemo, pericarditis
Chronic renal insufficiency
Myocardial strain–> CHF, PE
What are the ST elevation cut offs in men and women? Where must these elevations be?
Must be in two contiguous leads
Greater than or equal to 0.2 mV for men and 0.15 mV for women in leads V2 and V3, otherwise greater than or equal to 0.1 mV in other leads
What are the non invasive cardiac imagining techniques
Echo
MIBI
Cardiac CT angio
What are the invasive cardiac imaging techniques
Angiography
What test should you do in a low risk UA/NSTEMI
Exercise MIBNI (examines perfusion)
What test should you do in a high risk UA/NSTEMI
Early catheterization
What should you do in a STEMI?
if in a PCI capable hospital–> catheterization ASAP
Non-PCI hospital–> skip imaging and go straight to fibrinolysis
What are the general treatment principles of an MI and how do you achieve them?
- Increase oxygen supply
- -oxygen IF HYPOXIC
- -nitrates, morphine (vasodilation)
- -anti platelets–> ASA, plavix or alternative
- -anti coagulation–> heparin
- -relieve obstruction–> PCI, CABG, thrombolytics - Decrease demand
- -treat underlying cause of the increased demand (I.e sepsis)
- -beta blockers - Secondary prevention and myocardial recovery
- -statins
- -ACEi
- -MRAs
- -lifestyle
What is the treatment specifically for STEMI?
- Anti thrombotic therapy–> ASA, clopidogrel or ticagrelor, heparin or enoxaparin
- Reperfusion therapy–> PCI, thrombolytics (if STEMI), CABG if indicated
- Ancillary therapy–> nitro (anti angina), beta blocker, ACEi, MRA, statin, secondary prevention
What are the absolute contraindications to thrombolysis
- History of intracranial hemorrhage
- Ischemic stroke in the past 3 months
- Cerebral malformation or tumour
- Possible aortic dissection
- Bleeding diathesis
- Significant head trauma in past 3 months
What are some of the relative contraindications to thrombolysis
Poorly controlled BP Ischemic stroke more than 3 months ago Dementia Traumatic prolonged CPR Major surgery in past three weeks Internal bleeding in past four weeks No compressible vascular punctures Pregnancy Warfarin
What 4 meds should someone who suffered an ACS be discharged on and why
- ASA
- Beta blocker
- ACEi
- Statins
..each Med decreases future events by 25% (relative risk reduction) so best to be on all 4
Also..
Dual anti platelet therapy for more than 1 months for a bare metal stent, 1 year for a drug eluding stent and 1 year following ACS
What is the definition of thrombocytopenia
Normal platelets –> 150-400 (000) per mcl of blood
Thrombocytopenia is less than 150
a drop of more than 50% warrants investigation
What are the consequences of the following platelet levels
- Less than 50
- Less than 20
- Less than 10
- Surgical bleeding (100 for neuro surg)
- Risk of severe bleed with fever
- Risk of spontaneous bleeding (always look for neuro symptoms, need to rule out an intracranial bleed in these people when they present)
What is the overall approach to a thrombocytopenia?
- Increased destruction
- Decreased production
- Sequestration
- Other
What causes of thrombocytopenia fall under the “increased destruction” category?
- Non immune–>
MAHAs
Infection
Meds and toxins - Autoimmune–>
Immune thrombocytopenic purpura (ITP)
Heparin indicted thrombocytopenia
Name the MAHAs
Thrombotic thrombocytopenic purpura (TTP)
Hemolytic uremic syndrome (HUS)
Disseminated intravascular coagulation (DIC)
HELLP syndrome
Vasculitis and scleroderma crisis
Hypertensive crisis
Mechanical (mechanical heart valves etc)
Name the autoimmune causes of increased platelet destruction
ITP
HIT
What are the three categories of decreased production of platelets causing thrombocytopenia
- Hypo cellular
- Hyper cellular
- Bone marrow replacement or infiltration
What are the hypo cellular causes of decreased platelet production
Aplastic anemia Meds, toxins, substances Infection (sepsis, viral I.e HIV, parvovirus etc) Vitamin B12 and folate deficiency Liver cirrhosis Autoimmune disorders
What are the hyper cellular causes of decreased platelet production
MDS
Leukaemia and lymphoma
Multiple myeloma
HLH
What are the bone marrow replacement/infiltration causes of reduced platelet production
Myelofibrosis
Granulomas (TB, fungal, sarcoidosis)
Solid organ malignancies (mets breast, prostate, liver)
Haematological malignancies
What causes increased sequestration of platelets
Splenic pooling due to spenomegaly (I.e portal HTN)
What are the “other” causes of thrombocytopenia
Psueothrombocytopenia–> platelets clump in tube
Dilutional thrombocytopenia –> post transfusion of a large volume of pRBCs (usually more than 10 units)
What causes TTP?
Decreased ADAMTS13 protease activity–> can’t cleave the huge VWF multiverse on endothelial cell surface–> platelets stick to the endothelial surface–> huge clumps of platelets–> messes up the RBCs coming through–> SCHISTOCYTES and consumptive thrombocytopenia but NO activation of coagulation cascade (therefore coags normal)
What is the clinical Pentad of TTP and how many do you need for a diagnosis
Need 2 of-- Thrombocytopenia MAHA Renal failure Fever Mental status changes
What are some conditions associated with TTP
Infection--HIV, ecoli Autoimmune conditions Pregnancy Malignancy Drugs (rare)
What is the treatment for TTP
Aspirin
Steroids
FFP–> this has ADAMTS13 in it so it can go around cleaving the big VWF clumps
Definitive therapy is PLEX (plasma exchange)
TTP is a medical emergency and mortality without treatment is about 90% (with tx is 20)
What is the classic triad of HUS
MAHA
Thrombocytopenia
Acute renal failure
**associated with shiga toxin produced by ecoli
What is the precipitating factor in DIC
Activation of the coagulation cascade –> leads to thrombosis in the micro vasculature
- -> ischemia of end organs–> multi organ failure
- -> MAHA–> SCHISTOCYTES
- -> consumption of platelets AND FACTORS–> tcp AND COAGULOPATHY –> both clots and bleeding
What precipitates DIC
Trauma Infection Malignancy Obstetrical complications Toxins (snake bites)
Describe acute DIC
Severe coagulopathy with diffuse bleeding, ARF, hepatic dysfunction, ARDS
Describe chronic DIC
Milder bleeding
Arterial and venous thrombosis with malignancy
How can you differentiate DIC from TTP
Both have low platelets and large platelets and schistocytes on smear
TTP–> many schistocytes on smear, normal fibrinogen, normal INR/PTT
DIC–> fewer schistocytes on smear, low fibrinogen and high INR/PTT
What is primary ITP?
Can’t ID underlying cause
What is secondary ITP
Caused by
Drugs (I.e heparin)
Infections (HIV, EBV, CMV, HCV, H pylori)
Malignancy (CLL, lymphoma)
Autoimmune (SLE, anti phospholipid antibody syndrome)
Alloimmune (post transfusion)
What is the only cause of single digit platelets that you will likely see?
ITP
What are the symptoms of ITP
Petechiae
Purpura
Easy bruising
Usually very low platelet count, always less than 100 often less than 10
What is the most common (perhaps only) cause of isolated thrombocytopenia (no other cell lines affected at all)
ITP
How do you diagnose ITP
Isolated thrombocytopenia
VERY low platelets
Large platelets on peripheral smear
*diagnosis of exclusion
What must you rule out before dx of ITP
MAHA
Secondary causes
How’d you treat ITP
Prednisone--works in 1-2 weeks IVIG--works in 1-2 days Rhogam (for Rh+ pts) New TPO agonists Rituximab Splenectomy
What is HIT?
HIT type 1–mild tcp within the first two days of starting heparin, counts return to normal while the patient is still on heparin (due to platelet clumping)
HIT type 2–5-10 days post starting heparin, more serious form caused by antibodies targeting heparin and PF4 complex on platelets–> high risk of thrombotic complications (DVT, PE)
–will likely see lesions at puncture site
What is the treatment for HIT
Stop heparin
Start alternative anticoagulant–> argatroban, fondaparinux are not approved for use in HITT but are often used due to expert consensus
DO NOT start warfarin until substantial platelet recovery
What should you ask on history of tcp?
- Timing of platelet count drop and other cell lines involved
- Decrease production–>
- -recent infection (BM suppression? Secondary ITP?)
- -history of autoimmune diseases
- -detailed Med history
- -EtOH intake, nutritional status
- -history of liver disease
- -history of constitutional symptoms, malignancies, malignancy screening
- -history of granulomatous disorders, TB exposure - Increased destruction–>
- -history of HIV, HBV, HCV
- -history of h pylori
- -history of heparin exposure
- -history of DIC triggers
- -history of pregnancy, meds, autoimmune disease (TTP triggers)
- -history of diarrhea (?HUS) - Abdo pain/distension or early satiety for splenomegaly
- Consequences of the top–>
- -mucocutaneous bleeding (nose, gingiva, GI, easy bruising)
- -neuro symptoms (ICH)
- -history of bleeding with surgery, childbirth, dental work
- -transfusion history
What should you look for on exam for tcp?
General
H&N–> orzo pharyngeal petechiae, SLE rash, alopecia, pupils
CVS–> murmur (MAHA)
Abdo–> splenomegaly, tenderness, findings of chronic liver disease
Derm–> bruising, petechiae, bleeding skin, rashes
MSK–> joint effusions, thrombosis
Neuro–> CN II-XII, gross sensory and motor (ICH)
Lymph nodes–> H&N, axillary, inguinal
What labs would you order to investigate the following causes of tcp–
- MAHAs (HUS/TTP/DIC) overall
- DIC
- HUS/TTP
- Total/direct bilirubin, LDH, haptoglobin, peripheral smear (schistocytes), BUN and Cr (ARF)
- INR, PTT, D-dimer, fibrinogen level
- 5 Cardinal features, peripheral smear
What labs would you order to investigate the following causes of tcp–
- HIT
- ITP
- Calculate 4T score
2. Large platelets, isolated tcp
What labs would you order to investigate the following causes of tcp–
- Infection
- Malignancy
- Autoimmune
- HIV and hepatitis serology, urea breath test
- Peripheral smear, LDH, SPEP, age appropriate screening
- If suggested by clinical features, order ANA
What labs would you order to investigate the following causes of tcp–
- Bone marrow disease
- Liver disease (malignancy)
- Hypersplenism
- SPEP/UPEP, calcium, retics, B12, MCV, blast forms (leukaemia), teardrop (myelofibrosis), BM biopsy if still on Ddx (older patient, B sx, no other cause)
- LFTs and liver enzymes
- Physical exam or abdo U/S
Ddx peri umbilical or diffuse abdo pain
AAA
Ischemic bowel (secondary to underlying atherosclerotic disease or arterial embolism from Afib or valvular disease)
Bowel obstruction
Pancreatitis
Gastroenteritis
Metabolic disturbances
Ddx RUQ pain
Cholescystitis
Biliary colic
Hepatitis
Pyelonephritis
Ddx RLQ pain
Appendicitis
Nephrolithiasis
Crohn’s disease
Ovarian cyst or torsion
Ectopic pregnancy
PID
Testicular torsion
Inguinal herniation
DDx LUQ pain
Splenic rupture or infarct
Pyelonephritis
LLL pneumonia
Pancreatitis
DDx LLQ pain
Diverticulitis
Nephrolithiasis
IBD
Ovarian cyst/torsion
Hernia
Testicular torsion
What should you ask on history for abdo pain?
Changes with food?
Changes with position?
Fevers, chills, sweats?
N/V/D?
What would you expect on history for PUD
Pain diminishes with meal, gets worse after fatty meals
What would you expect on Hx and imaging for perforated viscus??
Sudden onset
Air under diaphragm on plain film
What would you expect on history for peritoneal irritation
Moving slowly, hunching forward to avoid jarring
What would you expect on Hx, physical for appendicitis? How to dx?
Starts vague, cramp like abdo pain that moves to RLQ and becomes sharper and more intense
Rebound tenderness, pain at mcburney’s, rovsings, obturator
Dx with CT
What would you expect on Hx and physical for diverticulitis
LLQ pain
Rebound tenderness
Dx with CT
What would you expect on history for biliary colic? What test would you order?
Severe, aching, steady pain in RUQ or epigastrium, lasts 1-4 hours, may be associated with meal
Amylase–> mild increase
What would you expect on history, physical for cholescystitis? What would you order for tests and imaging?
Persistent pain associated with fever and may radiate to R scapula
Murphys sign positive
Include ALP/GGT/Bili (cholestatic picture is increased bili and ALP)
On US–> thickened gallbladder, sonographic murphys, pericholecystic fluid
What would you expect on history, physical for pancreatitis? Workup?
Epigastric/peri umbilical pain, radiates to back, relieved with sitting, Hx of recent alcohol use
++ pain in RLQ, bowel sounds absent
Lipase
What would you expect on history, physical for ischemic bowel? Workup?
Sudden and severe onset
Hx Afib
Lots of pain in epigastrium and peri umbilical areas
Bowel sounds absent
Include lactate, lytes, amylase
Do CT
What would you expect on Hx for bowel obstruction?
Cramps mid abdominal pain Paroxysms History of abdo surgery Absence of recent BMs Absence of flatus
What would you expect on history for nephrolithiasis?
Begins gradually then escalates to severe pain in 20-60 min with flank pain radiating to groin or testicle
Hematuria on UA
What would you expect on history for AAA? On exam?
Pain radiates to back
History of vascular disease
Palpable, pulsating mass with diminished peripheral pulses
What would you expect on history, physical and labs for liver disease/hepatitis?
RUQ pain
Jaundice
Marked increase in LFTs, transaminitis (AST, ALT)
What would you expect on history and exam for gastroenteritis? What do you do?
N/V/D
Usually benign, diffuse tenderness
Observation, resuscitation with fluids as necessary
What would you expect on history and workup for DKA?
Abdo pain, nausea, vomit
Ketouria
Anion gap acidosis
What is a mnemonic for the causes of diarrhea?
MISO
Motility
Inflammatory (bloody)
Secretory
Osmotic
What are the Motility causes of diarrhea
Hyperthyroid Diabetic neuropathy Bacterial overgrowth IBS Scleroderma
What are the inflammatory causes of diarrhea
- Infections (invasive)–> salmonella, shigella, campylobacter, EHEC, EIEC, C diff, vibrio, yersinia
- Inflammatory–> UC, Crohn’s, ischemia, radiation, toxic
What are the secretory causes of diarrhea
- Infections (non invasive)–> viral (rotavirus, norovirus), vibrio, cholera, staph, b cereus, ETEC, EPEC, giardia, cryptococcus, amoeba
- Neuro endocrine–> carcinoid tumours, VIPoma, calcitonin excess, gastrinoma
- Meds–> laxatives, PPIs
What are the osmotic causes of diarrhea
- Maldigestion or malabsorption –> pancreatic insufficiency, celiac disease, lactose intolerance
- Medications–> antacids, antibiotics, Mg, lactose, sorbitol, colchicine, metformin
What should you ask on a history of diarrhea
Characterize onset, duration, frequency, volume, floating
Bloody versus non bloody
Abdo pain or weight loss
Sick contacts, travel, food, Med changes, swimming, camping
PMHx of DM, hyperthyroid, IBS, lactose intolerance, bowel surgery
What should you look for on physical exam of patient with diarrhea
Vitals Volume status Body weight Abdo tenderness Rectal exam for FOB
What labs would you order in a patient with diarrhea
CBCD, lytes, urea, Cr, lactate
–> if chronic diarrhea, add TSH, anti TTG antibody (celiac) + IgA level, andomysial antibody
Stool sample for C&S, O&P, c diff toxin, viral culture
Fecal osmotic gap
Fecal testing for giardia toxin
CTabdo if indicated
Endoscopy
How do you treat diarrhea
Depends on the cause
Symptom control with IV fluids
Anti diarrheals if not inflammatory diarrhea–> loperamide
How do you treat shigella, campylobacter, ecoli diarrhea
Levofloxacin
How do you treat vibrio cholera diarrhea
Tetracycline or doxycycline
How do you treat cyclospora diarrhea
Septra
How do you treat c diff, giardia, entamoeba diarrhea
Metronidazole
What are the SECSY bacteria
Shigella Ecoli Campylobacter Salmonella Yersinia
+c diff, entamoeba histolytica
INVASIVE INFECTIOUS
How do you treat infections with the SECSY bacteria?
Cipro
How do you treat IBD
5-ASA, corticosteroids, immunosuppressants
Ddx of neutrophilia (left shift)
- Infection–> usually bacterial
- Inflammation–> MI, PE, burns
- Neoplasm–> myeloproliferative neoplasm
- Drugs and toxins–> corticosteroids, beta agonists
- Stress–> release of endogenous corticosteroids and catecholamines
- Marrow stimulation–> hemolytic anemia, ITP
- Asplenia–> surgical, SCD
Ddx lymphocytosis
- Infection–> usually VIRAL
- Autoimmune–> RA
- Neoplasm–> leukaemia (CLL), lymphoma
Ddx monocytosis
- Infection–> TB, listeria, rickettsia, fungi, parasites
- Inflammation–> IBD, sarcoidosis, collagen vascular disease
- Neoplasm–> Hodgkin lymphoma, leukaemia
Ddx eosinophilia
- Infection–> usually parasitic
- Allergic–> drugs, asthma, eczema
- Neoplasm–> Hodgkin lymphoma, CML
Ddx basophilia
- Neoplasm–> MPN, HL
2. Inflammatory/allergy–> IBD, chronic airway inflammation
What should you ask on history in a leukocytosis?
Infection–> fever, chills, sx of infective focus
Cancer–> night sweats, weight loss, thrombocytopenia/anemia
Autoimmune–> joint pain, diarrhea, abdo pain, signs of SLE
Meds, allergies, possible exposures
Investigations for a leukocytosis
CBCD Peripheral smear Lytes BUN Cr Glucose
If suspect mi–> troponin, ECG
Pan cultures
Autoimmune workup–> ANA, RF, ANCA
Imaging–> CXR, CT, PET, US lymph nodes, echo
Viral causes lymphadenopathy
HIV EBV CMV HSV VZV Hepatitis
Bacterial causes of LAD
Generalized–> TB, syphilis
Localized–> staph, strep, cat scratch
Fungal/parasitic causes of LAD
Histoplasmosis
Toxoplasmosis
Immune related causes of LAD
Autoimmune–SLE, RA, scleroderma
Serum sickness
Neoplastic nausea of LAD
Lymphoma
Leukaemia
Metastatic CA
Infiltrative causes of LAD
Sarcoidosis
Amyloidosis
What to ask on Hx in LAD
Infective ROS Malignancy ROS Hx autoimmune disease--joint swelling, SLE sx Risks for HIV, hepatitis etc Pancytopenia
What factors favour doing a lymph node biopsy in the setting of LAD
Older than 40
LN bigger than 2cm
Greater than 1 mo duration
ALWAYS biopsy a supraclavicular LN as it is always abnormal
Name the primary epilepsies
Partial (simple, complex, secondarily generalized)
Generalized (absence, generalized tonic-clinic, myoclonic, atonic, tonic, clonic)
Unknown (epileptic spasms)
Name the structural causes of unprovoked epileptic seizures
Stroke (infarction)
Head trauma
Brain tumours
Neuro-degenerative disorders
Name the infectious causes of unprovoked epileptic seizures
Encephalitis
Name the congenital causes of unprovoked epileptic seizures
Neuronal migration errors and cortical dysgenesis
Vascular malformations
Name drugs that lower the seizure threshold
Bupropion
Theophylline
Isoniazid
Imipenem
High dose penicillin
Meperidine
Withdrawal from what substances can cause provoked seizures?
Alcohol
Benzodiazepines
Overdoses on what substances can cause provoked seizures?
Methanol
Ethylene glycol
TCAs
Which illicit drugs can cause provoked seizures (even if not OD)?
Cocaine
Amphetamines
LSD
Name the metabolic causes of (provoked) seizures
Hypoglycaemia
Non ketotic hyperglycaemia
Hyponatremia
Hypocalcemia
Uremia
Hypoxia (cerebral anoxia)
Hyperthyroidism
Infectious causes of provoked seizures
Meningitis
HSV encephalitis
Febrile seizures
What relatively common heart condition can cause provoked seizures
Arrhythmias
What conditions can mimic seizures
Syncope TIA Migraine BBPV Hypoglycaemia Sleep disorders (narcolepsy, OSA) Periodic paralysis
What is the pathophysiology of generalized seizures
Engages the cortex bilaterally, with loss of consciousness
What is the pathophysiology behind focal seizures without impairment of consciousness or awareness
Originate in one hemisphere
Possible motor, sensory, autonomic or psychic symptoms with sparing of consciousness and awareness
Used to be known as “simple partial seizure”
What is the pathophysiology behind focal dyscognitive seizures
Originate in one hemisphere
Possible motor, sensory, autonomic, psychic symptoms with IMPAIRED consciousness or awareness
Used to be known as a “complex partial seizure”
What is the pathophysiology behind a focal evolving to bilateral convulsive seizures
Originates in one hemisphere but evolves to engage the cortex bilaterally
What does a clonic seizure look like
Jerky contractions, rhythmic
What does a tonic seizure look like
Muscle stiffening
What is the definition of epilepsy
Any one of the following 3 criteria:
- 2 or more unprovoked seizures more than 24 hours apart
- 1 unprovoked seizure with probability of another seizure more than 60% over the next 10 years (i.e presence of a structural lesion associated with high risk for seizure recurrence)
- Diagnosis of epilepsy syndrome
What is status epilepticus
5 or more minutes of continuous seizure activity or more than two discrete seizures without complete recovery of consciousness in between events
What are some complications that can arise due to seizures
Seizure related injuries Aspiration pneumonia Neurogenic pulmonary edema Hypoxic brain injury Cardiac injury Rhabdomyolysis (leading to acute renal failure and hyperkalemia) Lactic acidosis Sudden unexpected death in epilepsy (SUDEP)
What should you ask on history for a seizure
When was the first seizure
Prodrome
Aura
Ictal symptoms
Post ictal period
Diurnal variation
History suggestive of missed seizure (I.e waking up with sore muscles, blood in mouth or urinary incontinence)
Precipitants (sleep deprivation, skipped meals, stress, messes, alcohol, missed medications, medication withdrawal)
Maximum seizure free period
Seizure types
Related injuries
Driving
Employment
What labs would you order to work up a seizure
CBCD, lytes, urea, Cr, glucose Ca, Mg, PO4 Liver enzymes, bilirubin, albumin CK, troponin TSH INR, PTT
**PROLACTIN–> acute increase in 10-20 min after generalized tonic clonic seizure, low sensitivity
What imaging would you order in the setting of a seizure
CT head
MRI
What other tests might you order to workup a seizure
EEG with or without sleep deprivation
Order for unprovoked or recurrent seizures (best done within 24 hours of seizure onset)
Consider sleep deprived EEG to increase yield of detecting epileptiform activity/focal abnormality
–Also, CXR if suspect aspiration and LP if suspect meningitis or encephalitis as a cause of the seizure
What is an aura
Focal seizure with subjective sensory or psychic phenomenon
What is a Jacksonian March
Focal motor seizure of primary motor cortex which produces clonic activity in the contra lateral side of the body
Rhythmic activity spreads to adjacent areas (I.e fingers to wrist to arms)
What is Todd’s paralysis
Hemiparesis or hemiplegia following a seizure, which suggest focal onset
What can EEG be used to diagnose
Useful for epilepsy (40-50% sensitivity, high specificity)
Metabolic and toxic encephalopathies
Herpes encephalitis
Subacute sclerosing panencephalitis
Prion diseases
How do you manage status epilepticus
ABC
Oxygen
IV access
STAT investigations (ABG, CBCD, lytes, Cr, glucose, Mg, Ca, PO4, toxic screen, anti epileptic drug level)
Glucose if hypoglycaemic –> thiamine in 50% dextrose IV
FIRST LINE–> lorazepam IV
Second line–> phenytoin IV
Third line–> midazolam
Fourth line–> anesthetic doses of propofol IV, need to intubate
**phenytoin and benzodiazepines are incompatible with same IV use, will precipitate if used in same line; use separate IV sites
What do you use for acute seizure control
Benzodiazepines (lorazepam IV) Anti epileptic (phenytoin... Or phenobarbital, carbamazepine, valproate)
IF EtOH WITHDRAWAL–> add thiamine
*do not use same IV for benzodiazepines and phenytoin
How do you manage seizures long term
Valproic acid–titration up to typical daily dose of 750-2000 mg PO daily
–most effective
Lamotrigine–titration up to typical daily dose of 100-400 mg
Topiramate–titration up to typical daily dose of 200-400 mg
Keppra
Carbamazepine
Gabapentin
What ministry do you need to check with if you have a patient with seizures
Motor vehicles–may have to report
Do you start anti seizure medications in a first time seizure?
If there is no structural lesion, no physical findings, and normal EEG, usually do not need to start antiseizure medications
Risk of recurrence after first seizure is 30-60%
Risk after second seizure is 80-90%
When may you consider stopping epileptic meds
After a seizure free period of 2-5 years
What are the top 5 drug induced seizure etiologies
Isoniazid–treat with pyridoxine
Theophylline–>supportive tx
Oral hypoglycemic agents–treat with glucose with or without octreotide and glucagon
Carbon monoxide–supportive tx and oxygen
Bupropion–supportive tx
Define Alzheimer’s
General sequence of changes include mood alterations, and slow, progressive cognitive decline
Primarily affects memory, language and visuospatial domains early on
Early motor symptoms are rare but may have apraxia later
Loss of functional autonomy, neuropsychiatric manifestations, Parkinsonism may be seen I more advanced stages of disease
CT may show white matter change
Mostly a diagnosis of exclusion but accounts for about 60% of dementia so
Define vascular dementia
Acute STEPWISE or slow progressive decline
May have focal neurological deficits
MMSE patchy
CT may show white matter change
Pure vascular dementia is uncommon, more frequently occurs along with Alzheimer’s like dementia (mixed vascular)
Define Parkinson’s dementia
Parkinson’s disease diagnosed for more than a year prior to cognitive onset
Slow decline
Parkinson’s patients have 6x increased risk of dementia
Define Lewy body dementia
Progressive memory decline
Parkinsonism
Visual hallucinations
Fluctuating cognition (especially attention/alertness)
Visuospatial domain often markedly impaired
Supportive features–> adverse hypersensitivity to typical antipsychotic meds, syncope, falls, delusions, sleep disturbance
Define frontotemporal dementia
Age usually less than 60
Behavioural symptoms noticeable before cognitive impairment–> disinhibited or passive presentation, impaired judgment, significant social indifference, declining hygiene, prominent language deficits but amnesia less noticeable early on
Early primitive reflexes/incontinence
Late akinesia, rigidity, tremor
Impaired executive function
**MMSE may be normal
CT shows FRONTO TEMPORAL ATROPHY
What are the potentially reversible causes of dementia
- Metabolic–> alcoholism, vitamin B12 deficiency, hypothyroidism
- Structural–> normal pressure hydrocephalus (NPH), subdural hemorrhage, neoplastic, vascular
- Infectious–> chronic meningitis, HIV, neurosyphilis, Whipple’s
- Inflammatory–> vasculitis, hashimotos encephalitis, MS
What conditions does dementia mimic?
Depression
Delirium
Developmental disorders
Age associated memory impairment
What physical findings might you expect to find in
- Alzheimer’s
- Vascular
- Fronto temporal
- Relatively normal
- Focal neuro deficits
- Primitive reflexes, disinhibited or passive
What MMSE findings might you expect to find in
- Alzheimer’s
- Vascular
- Fronto temporal
- Memory recall affected early on, then language and visuospatial deficits
- Patchy changes
- May be normal
What changes might you see on CT head in
- Alzheimer’s
- Vascular
- Fronto temporal
- White matter changes
- White matter changes
- Frontotemporal atrophy
What labs might you order to work up dementia
CBCD, lytes, creatinine, glucose, calcium, TSH, vitamin B12
Imaging CT head
Could also do:
AST, ALT, ALP, bilirubin, RBC folate, VDRL, HIV serology, urine collection for heavy metals
What are the DSM V criteria for a major neuro cognitive disorder
- A decline in one or more than one cognitive domain–> learning and memory, language, executive function, complex attention, perceptual abnormalities, social cognition
- Cognitive deficits must impair at least one IADL
- Cognitive deficits do not occur during delirium and are not better explained by another psychiatric disorder
What is the Hachinski Ischemic Score
A scoring system used to help distinguish between Alzheimer’s and vascular dementia
Includes points like fluctuating course, depression, stepwise progression etc
Score of less than 4 suggests Alzheimer’s is likely
A score of more than 7 suggests likely vascular dementia
What does an abnormal clock drawing test suggest
Dementia
LR +5.3
(Normal clock drawing is not useful as half of demented patients can produce a normal clock)
What are the criteria for ordering a CT head in a dementia patient
Age less than 60
Rapid onset of 1-2 months
Unexplained decline in cognition or function
Dementia of short duration–less than two years
Unexplained neuro symptoms
Early incontinence or gait problems (NPH)
Recent head trauma
History of cancer or bleeding disorder
New localized signs
Management of dementia–what are the different aspects to consider?
- Risk reduction
- Disease management
- Symptoms management
- Tube feeing
What can be done for risk reduction in dementia
Anti hypertensive
Dyslipidemia treatment
What can be done for disease management for dementia
Start an anticholinesterase for Alzheimer’s (donepizil, rivastigmine_
–avoid if has seizures, cardiac conduction problems, significant asthma, COPD or recent GI bleed
Memantine may be used as a single agent or as add on therapy to above
What can be done for symptom management in dementia
Treat problem behaviours with non pharmacological and pharmacological approaches ( trazodone, atypicla antipsychotics)
Treat co existing depression
Is tube feeding recommended in dementia?
Generally not in advanced dementia due to increased risk of complications without evidence of clinical benefit (I.e no increase in survival or quality of like or prevention of aspiration pneumonia_
What causes normal pressure hydrocephalus (NPH)
Inflammation and fibrosis of the arachnoid granulations–> decreased absorption of CSF–> hydrocephalus–> normal opening pressure but elevated pressure over peri ventricular white matter tracts
Idiopathic or secondary to subarachnoid hemorrhage, chronic meningitis etc
How does NPH present?
Classic triad of gait apraxia (magnetic gait as feel are stuck to floor), urge incontinence, cognitive decline
May also have postural instability, lower extremity spasticity, hyperreflexia, extensor plantar responses
How do you diagnose NPH
Clinically and with MRI
Improvement of gait or cognition 1 hour after removal of CSF helpful for diagnosis (Fisher test, PPV of 90-100%)
Treatment for NPH
LP, shunts
What are the Parkinson’s plus syndromes?
Progressive supra nuclear palsy
Etc…
How does CJD present?
Rapid progression, characteristic EEG, myoclonic jerks, expected death within 6-12 months
How does huntington’s dementia present?
Autosomal dominant with incomplete penetrance
What is the mnemonic for decreased LOC/delirium?
DIMS Drugs Infection Metabolic Structural (R--retention)
What is the mnemonic for the drug causes of delirium?
ABCD
Alcohol (intoxication and withdrawal) anticholinergics (atropine, benztropine) antidepressants (SSRIs, TCAs) analgesics (opioids, NSAIDs, steroids) antibiotics (penicillins, quinolones, isoniazid, rifampin) Antihistamines (cimetidine, ranitidine)
Benzodiazepines and barbiturates (intoxication and withdrawal)
Cardiac (amiodarone, beta blockers, digoxin, diuretics) Dopamine agents (amantadine, bromocriptine, levodopa)
What are the metabolic causes of delirium
Organ failure–> hepatic, anorexia, hypothyroidism, thyrotoxicosis, hypoxia, hypercapnea, hypothermia, hypertensive
Electrolyte imbalance–> ketoacidosis, hyper or hypoglycemia, hyponatremia, hypernatremia, hypomagnesemia, hypercalcemia
What are the structural causes of delirium
- Hemorrhage–> subarachnoid, epidural, subdural, intracerebral
- Stroke–> basilar
- Tumour
- Abscess
Why is delirium so common in the hospitalized elderly?
Limited reserve so easy to tip over into delirium
What are the subtypes of delirium
- Hyperactive delirium–> characterized by agitation and/or hallucinatory symptoms
- Mixed delirium–> variable course with alternating hyperactive and hypo active features…majority of patients fall into this category
- Hypo active delirium–> characterized by excessive drowsiness and decreased LOC, may mimic depression
How does the onset differ between
- Delirum
- Dementia
- Abrupt
2. Insidious
How does the course differ between
- Delirium
- Dementia
- Fluctuating, usually reversible
2. Slowly progressive and usually irreversible
How does the duration differ between
- Delirium
- Dementia
- Days to weeks
2. Years
How does the level of consciousness differ between
- Delirium
- Dementia
- Hyper or hypo active
2. Affected in late stages
How does attention span differ between
- Delirium
- Dementia
- Often affected
2. Affected in late stages
How does memory differ between
- Delirium
- Dementia
- May be affected
2. Usually affected
What tool can be used to assess delirium?
The Confusion Assessment Method (CAM)
Positive test argues strongly for delirium (LR +10.3) and negative test argues against it
Positive test requires both major criteria 1 and 2 and either of the minor criteria 3 and 4
- Acute onset and fluctuating confusion–> abnormal behaviours come and go with variable severity
- Inattention–> difficulty focusing/difficulty following conversation
- Disorganized thinking–> rambling, irrelevant, illogical conversation
- Sensorium change (altered LOC)–> agitated, hyper alert, lethargic, stuporous, or comatose
Also should get a baseline MMSE to monitor
What investigations should you get to work up delirium
- Labs–> CBCD, lytes, urea, Cr, glucose, calcium, UA
- Imaging–> CXR, CT head
- Micro–> urine C&S, blood C&S (if any fever)
- Metabolic workup
- Cardiac workup
- Seizures workup
- Drug OD workup
- Meningitis workup
What is the metabolic workup for delirium
TSH if suspect hyper or hypothyroid
AST, ALT, ALP, bili, INR, PTT, ammonia if suspect liver disease
Magnesium
Phosphate
What is the cardiac workup for delirium
ECG
CK
Troponin if suspect ACS
What is the seizure workup for delirium
EEG
What is the drug OD workup for delirium
Med serum levels
Alcohol levels
Serum osmolality
What is the meningitis workup for delirium
LP
What should you do if delirium persists and no cause found on workup
Think through diagnosis again
Ask caregivers about prior baseline–> pre existing sun downing?
Consider dehydration, depression, urinary/fecal retention, alcohol or benzo withdrawal, abscess, sleep deprivation, environmental factors
Inadequate pain control has also been suggests as a precipitant of delirium
How can you prevent delirium
Ensure adequate oxygen, fluid and electrolyte balance Pain management Reduction in use of antipsychotics Bowel and bladder function Nutrition Early mobilization Prevention of post op complications Appropriate environmental stimuli Treatment of symptoms of delirium
How would you manage delirium overall (principles of treatment)
- Prevention
- Treat underlying cause
- Non pharmacological measures
- Pharmacological measures
How long does delirium take to resolve
Can take days/weeks to resolve been after the precipitating cause is removed and treated
What are some non pharmacological measures that can be used to treat delirium
Reduce noise Orient patient frequently Early mobilization Provide proper hearing and visual aids Provide clock/calendar and familiar objects and people Supervision for meals Restoration of day-night cycle (optimal light during day, dark at night) Avoidance of unnecessary interventions
What are some pharmacological treatments for delirium
- Neuroleptics–> for agitated patient–> haloperidol, loxapine, quetiapine etc
- Benzodiazepines–> may precipitate or worsen delirium and should generally be avoided except in patients with alcohol or benzo withdrawal or those with severe agitate delirium despite high doses of neuroleptics–> lorazepam
What causes T1DM
Autoimmune destruction of beta cells–> insulin deficiency
Affects 0.5% of world population
What causes T2DM
Peripheral insulin resistance, impaired regulation of hepatic gluconeogenesis, impairment of beta cell function (beta cell exhaustion and from glucose toxicity)
Affects 8% of US population but increasing in the young –> 35% lifetime risk for those born in year 2000
What are the risk factors for T2DM
Family history
Older age
Obesity
How does the first onset of T1DM usually present
Often presents with diabetic ketoacidosis–> N/V, polyuria, anion gap metabolic acidosis, ketones in blood and urine
How does T2DM usually present?
What end organ damage do we worry about?
Usually asymptomatic, discovered on routine testing
If symptomatic–> polyuria, polydipsia, polyphagia, fatigue, blurred vision, poor wound healing, recurrent candidiasis
Peripheral numbness–> neuropathy
Loss of vision–> retinopathy
Microalbuminuria, proteinuria–> nephropathy
Angina–> CAD
Claudication or impotence–> peripheral vascular disease
What should you look for on physical exam in the diabetic patient
- Fundoscopy in office, annual dilated pupil exam with slit lamp
- -> looking for non-proliferative retinopathy–> microaneurysms, hard exudates (vascular leakage), soft exudates (Ischemic injury), macular edema
- -> looking for proliferative retinopathy–> neovascularization of the retina or optic disc - Sensory–> vibration, light touch
- -> always check feet - Orthostatic vitals–> autonomic neuropathy
- Evidence of CAD–> increased JVP, S4, displaced PMI, peripheral vascular disease (decreased peripheral pulses, bruits)
What is the Ddx for hyperglycaemia
- Diabetes
- Drugs (corticosteroids, thiazides diuretics, protease inhibitors)
- IV fluids (D5)
- Other endocrine–> acromegaly, cushings, pheochromocytoma
- Stress (via catecholamines release)
- Other–> hemochromatosis, pancreatic exocrine insufficiency (CF, acute or chronic pancreatitis)
How do you diagnose diabetes?
- Fasting glucose higher than 7 mmol/L
- 2 hour OGTT higher than 11.1 mmol/L
- HbA1c higher than 6.5%
- Random glucose higher than 11/L WITH SYMPTOMS
What is a normal fasting glucose
4-7 mmol/L
What is “pre diabetes”
Fasting glucose 6.1-6.9, OGTT 7.8-11, HbA1c 6-6.4%
What labs would you order in the diabetic patient
CBC
Iron studies (hemochromatosis)
Lipase (pancreatitis)
Urine micro albumin and creatinine annually
How do you treat T2DM
- Biguanides (metformin)
- Sulfonylureas (glyburide, gliclazide)
- Meglitinides (repaglinide)
- Thiazolidinedions (pioglitazone)
- Alpha-glucosidase inhibitors (acarbose)
- DPP4 inhibitors (linagliptin-trajenta)
- SLGT2 inhibitors (saxenda, canafligozin)
- GLP-1 analogues (liraglutide)
What do biguanides do? SEs?
Metformin
“Insulin sensitizing”
Inhibit hepatic gluconeogenesis and increase peripheral uptake of glucose
Very low incidence of lactic acidosis
SEs: GI (diarrhea). Avoid in patients with renal disease because is 100% really excreted and risk of lactic acidosis increases
What do sulfonylureas do? SEs?
Glyburide, gliclazide
Increase amount of insulin produced by the pancreas.
SEs: weight gain, hypoglycemia
What do meglitinides do?
Repaglinide
Increases insulin secretion
NOT really excreted so better for patients with renal disease
More expensive
What do Thiazolidinedions do?
Pioglitazone
Increase insulin sensitivity in the liver and muscle
Slightly less potent
Usually used in combo with older agents
Most expensive
SEs–fluid retention
What do alpha-gluconidase inhibitors do?
Acarbose
Inhibit absorption of carbs by preventing breakdown in small intestine
SEs: bloating, diarrhea, gas
Used in combination
What do DPP4 inhibitors do?
Linagliptin, trajenta
Increases GLP-1 (incretins) by inhibiting DPP4
How do you manage T1DM insulin therapy
Calculate 0.5 U/kg/day in T1–> T2 dose needs vary greatly
Short acting insulting–> regular and lispro–> used at times of meals
Intermediate insulin–> NPH and lente
Long acting insulin–> glargine–> basal insulin level throughout day especially at night (to suppress liver gluconeogenesis)
Can be given through numerous subQ injections or continuous infusion
What are the neuroglycopenic symptoms of hypoglycemia? What are the adrenergic symptoms?
- Neuroglycopenic–> CNS dysfunction–> headache, blurred vision, confusion, seizure, loss of consciousness
- Adrenergic–> epi release–> tachy, tachypea, diaphoresis, tremulousness, palpitations, anxiety
What is the difference between T1DM and T2DM
Basically, T1DM the problem is at the pancreas and in T2 it is as the tissue cells in the body
Why do you develop hyperglycemia in DKA/HHS
Insulin resistance (relative or absolute)
Increased glucagon
Increased catecholamines, cortisol, growth hormone
What is the major issue in DKA?
Ketoacidosis
Absolute insulin deficiency–> switch to using fats for fuel–> ketogenesis–> ketoacidosis
What is the major issue in HHS?
Osmotic diuresis
Relative insulin deficiency and increased in counter-regulatory hormones–> increased proteolysis, increased gluconeogenesis
Severe hyperglycemia
Glucose is an active osmole causing osmotic diuresis
How do the following differ in DKA vs. HHS
- Glucose
- PH
- HCO3
- Glucose–> DKA higher than 14//HHS higher than 33
- pH–> DKA less than 7.3 (acidosis)//HHS higher than 7.3 (non acidodic)
- HCO3–> DKA less than 15 (getting used up)//HHS higher than 18
How do the following differ in DKA vs. HHS
- Urine ketones
- Serum ketones
- Serum osmolality
- Urine ketones–> present in DKA//small in HHS
- Serum ketones–> present in DKA//none or small in HHS
- Serum osmolality–> variable in DKA//higher than 320 in HHS
How do the following differ in DKA vs. HHS
- Anion gap
- What symptoms are present?
- Anion gap–> higher than 12 in DKA//variable in HHS
2. DKA–> symptoms of ketoacidosis//HHS–> symptoms of osmotic diuresis
Why do people get DKA/HHS?
Almost always there is PRECIPITANT –> something that triggers the hormonal abnormalities
I.e increased catecholamines, increased cortisol, less insulin
What is the number one thing to do first when treating DKA?
GIVE FLUIDS
What are the general principles of treatment of DKA?
- Fluid resuscitation
- Avoidance of hypokalemia
- Correct the acidosis–> aim to CLOSE THE ANION GAP
- Maintain high/normal-glycemia (don’t bring BG down too much)
- Search for a precipitating cause
- Transition to SC insulin
- In kids, avoid cerebral edema
How do you manage fluid resuscitation in DKA/HHS?
- GIVE FLUIDS UP FRONT
- -> pretty much everyone can take 2L IVF - Then, run patients at 150-200cc/hr as most have significant fluid deficit
- Once euvolemia achieved, can switch to maintenance fluids
- NS usually used up from but not ideal–> worsens acidosis–> balanced salt solution preferable–> switch to hypotonic fluid if Na becomes elevated
What is the overall K balance in DKA/HHS?
Depleted
Due to osmotic diuresis and K+/ketoacid salt excretion
DKA–> 2-5mmol/kg deficit
HHS–> 4-6mmol/kg deficit
K is often normal on tests because it shifts out of cells due to acidosis, insulin deficiency and hyperosmolality
How do you manage K balance in DKA/HHS?
Monitor lytes q2-3h
- If initial K less than 3.3–> not NOT start insulin until K is corrected–> give 40mEq IV immediately
- If initial K 3.3-5, run IVF with K added (20-40 mEq in 1L)
- If initial K above 5, don’t need to add K to initial fluids–> know that it will likely drop precipitously once the acidosis is corrected
Why do we give insulin in DKA/HHS?
To CLOSE THE ANION GAP (not to lower blood glucose)
How much insulin do we give to treat DKA/HHS?
Insulin IV infusion at about 5-10u/hour (0.14u/kg/hr)
Monitor CBG q1h, lytes 2-3h
Goal is to close the anion gap
How do we titrate the insulin infusion based on blood glucose monitoring in DKA/HHS?
If AG is unchanged–> increased infusion
If AG decreasing–> can titrate the infusion down
If AG is still open but BG less than 15, START D5W
When do you start adding D5W to fluids in DKA/HHS?
If anion gap is still open but BG is less than 15, start D5W
What are the precipitating causes of DKA/HHS? What’s the memory tool?
The 7 Is:
*Insulin deficiency (“idiocy”)
*Infection–pneumonia, UTI, gastro etc
Iatrogenic–glucocorticoids
Inflammation–cholescystitis, pancreatitis
Ischemia or infarction–myocardial, cerebral, mesenteric, pulmonary
Intoxication–alcohol, drugs
Impregnation
What labs/investigations should everyone presenting with DKA get?
Thorough Hx/px Pan cultures CXR ECG Tox screen Liver enzymes, lipase Beta HCG (pregnancy)
What are the criteria for transitioning to SC insulin when managing DKA/HHS?
ANION GAP IS CLOSED
PH above 7.3, HCO3 above 15
Patient is tolerating normal diet (watch them eat!)
Daytime hours–> do not switch overnight
Ensure at least two hour bridge with subcutaneous insulin
Must start LONG ACTING as well as rapid or will go back into DKA
What is the recommended dosing for SC insulin after treating DKA/HHA?
- New DM1–> 0.5-0.8 units/kg/day
- Known DM1–> restart basal and prandial dose with or without sliding scale; start at lower dosing until you’re sure they’re eating well
- Known DM2–> estimate basal insulin at 0.3 u/kg/day and consider restart or oral agents
What should you bear in mind with treatment that is unique to HHS (versus DKA)
- More volume deplete–> fluids usually key treatment, must watch electrolytes as are also more K deplete
- Less acidodic–> need less insulin to close the anion gap
- Target a higher BG before assign D5W as these people tend to be used to running a bit hyperglycemic and may not be able to immediately handle normoglycemia
- Correct precipitating cause
What is a basic approach to an ABG interpretation?
- What is the “emia”–> acidemia versus alkalemia
- What is the “osis”–> respiratory versus metabolic
- Appropriate compensation?
- What is the anion gap?
- What is the delta delta?
Define shock
Inadequate tissue perfusion potentially resulting in end organ injury
List the types of shock
Hypovolemic
Cardiogenic
Obstructive
Distributive
Examples of causes of hypovolemic shock
Hemorrhage Dehydration Vomiting Diarrhea Interstitial fluid redistribution
Examples of causes of cardiogenic shock
Myopathic (ischemia, infarction)
Mechanical
Arrhythmic
Pharmacological
Examples of causes of obstructive shock
Massive PE (saddle embolus)
Pericardial tamponade
Constrictive pericarditis
Increased intra thoracic pressure (tension pneumo)
Examples of causes of distributive shock
Sepsis Anaphylaxis Neurogenic Endocrinologic Toxic
What should you ask on history in a patient with shock
Pay particular attention to the risk factors for sepsis (pna, UTI, recent chemo, SSTIs)
Blood loss
MI
PE (cancer, immobilization, calf pain, recent surgery)
General PMHx
Meds
What should you look for on physical of a patient with low BP/shock
Vital Assess volume status Cardiac and resp function Extremities Look for evidence of end organ dysfunction or hypo perfusion
What are you looking for on foot exam in a patient with shock? Why?
WARM feet–> vasodilation–> distributive shock–> give fluids and other vasopressors
COLD feet–> vasoconstriction–> cardiogenic vs. Hypovolemic vs. Obstructive vs. Late septic–> give fluids and consider inotropes especially if suspect cardiogenic
–also check troponin and consider echo
Describe how HR, BP, JVP, extremities respond in hypovolemic shock
HR increased
BP decreased
JVP down
Extremities cold
*look for visible hemorrhage or signs of dehydration
Describe how HR, BP, JVP, extremities respond in cardiogenic shock
HR low, normal or high
BP low
JVP high
Extremities cold
*bilateral crackles on chest exam
Describe how HR, BP, JVP, extremities respond in obstructive shock
HR up
BP down
JVP up
Extremities normal or cold
*depending on the cause, may see pulsus paradoxus, Kussmaul’s breathing, tracheal deviation
Describe how HR, BP, JVP, extremities respond in distributive shock
HR up or down
BP down
JVP down
Warm extremities
*look for obvious signs of infection or anaphylaxis
What investigations would you do in a patient presenting with shock
- Labs–> CBCD, extended lytes, urea, Cr, INR, PTT, liver enzymes, TSH, D dimer, lactate, CK, troponin, UA, random cortisol
- Micro–> blood, sputum and urine C&S
- Imaging–> depends on suspected source… CXR, AXR, echo, CT (I.e if abdo source suspected)
- ECG
- ABG
How do you manage shock acutely
ABC Oxygen oximetry monitoring IV fluid resuscitation Inotropes (dobutimine, milrinone) Pressors (norepi, phenylephrine) Re-vascularize or thrombolytics for Ischemic events
Define primary HTN
High BP in which all secondary causes are not present
Accounts for 95% of all cases
Genetic factors are though to contribute
Increased sympathetic output, angiotensin II and mineralocorticoids, renal injury may play a role
Define secondary HTN
Pathogenesis of increased BP is related to an identifiable underlying condition
What are the risk factors for essential HTN
Obesity
African American race
High salt intake (in salt sensitive patients)
Insulin resistance
High alcohol intake above 2 drinks per day
Family history–risk doubles if one parent is hypertensive
What is hypertension a risk factor for
Cerebrovascular disease CAD CHF Afib CKD PVD Dementia Erectile dysfunction
How common is white coat HTN
About 10% of adult population
How do you dx HTN
- Elevated BP at home, office or pharmacy
- Schedule a dedicated HTN visit… If above 180/110, has HTN
- If not…
A. and the patient has diabetes and an Automated office BP (AOBP) of above 130/80, proceed with further out of office measurement with an ABPM (or home series)… If above 135/80 as a daytime mean or above 130/80 as a 24 hour mean, they have HTN. If not, have white coat HTN
B. And the patient does not have diabetes, and has an AOBP of above 135/85 then proceed with out of office measurement with ABPM or home series. See above. If they meet the above criteria, they have HTN. If not, they have white coat HTN.
C. If the diabetic or non diabetic patient does not meet the above 130/80 // 135/85 criteria in the office on the dedicated visit, then they do not have HTN.
When should you order a 24 hour ABPM
All patients with a potential HTYN dx should be considered for ambulatory monitoring
Disadvantages are cost and lack of availability
What types of end organ damage would you want to asses for in a patient with HTN
- Cerebrovascular disease–> TIA/CVA, dementia
- Retinopathy
- Cardiac–> CHF, CAD, LVH
- Nephropathy–> albuminuria, CKD
- PVD–> intermittent claudication, ABI of less than 0.9, present of bruits
How can you elicit information about end organ damage in a patient w HTN on history
- Neuro–> transient monocular blindness (TIA), limb/facial weakness (CVA), severe headache (hemorrhage)
- Cardiac–> chest pain (CAD), Dyspnea, leg edema (CHF)
- Retinal–> vision loss
- PVD–> claudication, AAA
What are the grades of hypertensive retinopathy
1–> decreased artery to vein ratio
2–> focal arteriolar spasm
3–> FLAME HEMORRHAGES, cotton wool spots (Ischemic nerve damage), yellow exudates (plasma leakage)
4–> PAPILLEDEMA
What labs would you order to work up a hypertensive patient
UA Blood chemistry Fasting glucose and maybe HbA1c Fasting lipids Standard 12 lead ECG Urine ACR in patients with diabetes or CKD
What components make up the Framingham risk score
Age LDL cholesterol HDL cholesterol BP Diabetes Smoker
What do the different risk stratification levels in the Framingham score mean
Low risk–> less than 10% risk of non fatal MI or CHD death within next 10 years
Moderate risk–> 10-20% risk
High risk–> more than 20% risk
What are the non modifiable CV risk factors
Age
Male sex
Family Hx (less than 55 y males, less than 65 y female)
What are the modifiable CV risk factors
Smoking Dyslipidemia Dysglycemia HTN Abdominal obesity (>35 inches males, >40 inches females) Sedentary lifestyle Poor dietary habit
Why do we treat people younger than 60 with HTN
Reduces risk of stroke by 40%
Reduces risk of coronary event by 14%
Why do we treat patients older than 60 with HTN
Reduces overall mortality by 15%
Reduces CV mortality by 36%
Reduces incidence of stroke by 35%
Reduces coronary artery disease by 18%
What is the target BP in patients over 80
Less than 150 from the HYVET trial
What lifestyle modifications can help manage HTN
- Less than 2 g sodium per day
- Healthy diet with fruits and veg, low fat dairy, whole grains
- Regular physical activity
- Less than 14 drinks per week for men and 9 for women
- Maintenance of ideal body weight of BMI 18.5-24.9
- Waist circumference less than 102 cm for men and 88 for women
**most effective are exercise and dietary patterns
What are the indications for starting meds in a HTN patient
- dBP above 100 or SBP above 160 without macro vascular damage
- dBP above 90 in macro vascular damage or CV risk factors
- SBP above 140 in macro vascular damage
- SBP above 160 in seniors
What are the drugs used to treat HTN
Thiazides diuretics ACEi ARB Long acting CCB Beta blocker--not as first line in age 60 or older
Can use a combo of any two of these as first line therapy–often thiazide and ACEi
Make sure to check renal function with ACEi/ARB
CHEP says start initially with mono therapy
In a patient with HTN and stable angina what do you use?
Beta blocker
Long acting CCB
ACEi
In a patient with HTN and recent ACS what do you use?
Beta blockers
ACEi
In a patient with HTN and decreased LVEF what do you use?
ACEi
Beta blockers
Nitro/hydralazine
Aldosterone antagonist
In a patient with HTN and non diabetic CKD what do you use?
ACEi/ARB
Thiazide
Loop for volume control
In a patient with HTN and diabetes without nephropathy what do you use?
ACEi/ARB -or-
Thiazide -or-
ND-CCB
In a patient with HTN and diabetes with nephropathy what do you use?
ACEi/ARB then ND-CCB
Adverse effects of thiazides
Hypokalemia
Hyponatremia
Worsening gout
Adverse effects of non-DHP CCB
Bradycardia
Constipation
Adverse effects of DHP-CCB
Peripheral edema
Adverse effects of beta blocker
Fatigue, erectile dysfunction, bradycardia, depression
Name a CCB
Amlodipine
When do you start to consider secondary HTN may be a cause
Severe or resistant HTN (requiring more than 3 drugs to control)
HTN in the very old or the very young–> new onset HTN in the elderly or age less than 30 with no family history and no obesity
Sudden increase in BP when previously controlled
Flash pulmonary edema with elevated BP
What are the classes of causes of secondary HTN
Endocrine
Renal
Drugs
Other
Endocrine causes of secondary HTN
Primary aldosteronism
Cushing syndrome
Hyperthyroidism
Hypothyroidism
Pheochromocytoma
Symptoms of primary aldosteronism
Persistent hyperkalemia
Metabolic alkalosis
Symptoms of cushings
Cushingoid face
Easy bruising
Thinning skin
Centra obesity
Proximal muscle weakness
Symptoms of hyperthyroidism
Palpitations
Vision changes
Diarrhea
Heat intolerance
Symptoms of hypothyroidism
Weight gain
Cold intolerance
Constipation
Symptoms of a pheochromocytoma
Spells of tachy
Sweating
Headache
Pallor
Panic attacks
What are the renal causes of secondary HTN
Renal artery stenosis
Parenchymal–> CKD, polycistic kidneys
Glomerular–>GN
In what patient might you suspect renal artery stenosis
Acute rise in creatinine after ACEi/ARB
Moderate to severe HTN in patient with diffuse atherosclerosis
Repeated flash pulm edema
What are some drugs that can cause secondary HTN
NSAIDs–including “coxibs”
OCP
Sympathomimetics–> cocaine, oral decongestants
Steroid based–> prednisone, fludrocortisone, anabolic
Calcineurin inhibitors–> cyclosporine, tacrolimus
What are some “other” causes of secondary HTN
OSA–> snoring, daytime somnolence, headache, non restorative sleep
Coarctation of the aorta
How do you investigate for
- Pheochromocytoma
- Primary aldosteronism
- Cushings
- Hyper/hypothyroid
- 24 hour urine metanephrines
- Serum renin, aldosterone, hypokalemia
- 24 hour urine cortisol
- TSH
How do you investigate for
- OSA
- Coarctation of the aorta
- Renal artery stenosis
- Polycystic kidneys
- Overnight oximetry
- CXR, echo
- MR or CT angiogram, Captopril renal scan if eGFR is above 60
- Renal U/S
What is a hypertensive crisis
SBP above 200, dBP above 120
What is a hypertensive urgency
A hypertensive crisis that gets lower in 24-48 hours with NO end organ involvement
What is a hypertensive emergency
A hypertensive crisis with END ORGAN involvement
What are some signs of end organ involvement indicating a hypertensive emergency
Neuro--> encephalopathy, stroke Retina--> retinopathy Cardiopulm--> acute LV failure, pulm edema, aortic dissection, ACS Renal--> acute GN Other--> hemolysis
How does HTN affect cerebral blood flow auto regulation
Shifts the curve to the right so the range at which the brain is able to auto regulate is higher… Don’t want them to get too hypotensive actually
What oral agents can be used to manage a hypertensive emergency
Captopril–not with renal disease
Labetalol
Clonidine
Hydralazine
What IV agents can be used to treat hypertensive emergency
Work within minutes
Nitroprusside
NTG
Labetolol
Ddx of mono arthritis
ICU RN
Infectious Crystal Unclassified Rheumatologist (early stage... Unusual presentation) Neoplastic
Infectious causes of mono arthritis
Bacterial–> gonococci, staph, strep, syphilis, TB
Viral–> HIV, HBV, parvovirus, rubella, mumps, enterovirus, adenovirus
Fungal–> cryptococcus
OM
Crystal causes of mono arthritis
Gout
Pseudo gout
Unclassified causes of mono arthritis
Trauma
OA
Hemarthrosis –> coagulopathy, thrombocytopenia, trauma
Non arthritis–> bone (OM, avascular necrosis, fracture), soft tissue (tendinitis, ligament tear, bursitis)
Rheumatologist causes of mono arthritis
- Seropositive–> polymyositis, palindromic rheumatism, SLE, scleroderma, RA
- Seronegative–> psoriatic arthritis, enteric arthritis, ankylosing spondylitis, reactive arthritis
- Sarcoidosis, polymyalgia rheumatica
Neoplastic causes of mono arthritis
Chondrosarcoma
Osteoid osteoma
Mets
What is the most common cause of septic arthritis in sexually active adults without other risk factors (like immunosuppression)
50% is due to gonococcal infection
More common in women
Less destructive and better outcome than non gonococcal arthritis
What is a finding often found in gout
Tophi
How can you distinguish joint diseases from soft tissue injuries in your assessment of mono arthritis
Soft tissue–active ROM is affected while passive is not
Joint–both active and passive ROM is affected
What should you do to test if someone has septic arthritis
Tap the joint
Check synovial WBC count and percentage of PMNs as these provide the best utility while waiting for gram stain and culture
patients with mono arthritis have septic arthritis until proven otherwise!!!!*
What should you send arthrocentesis fluid for when assessing mono arthritis
3Cs
Cell count with diff
Culture and gram stain
Crystals
Does the presence of crystals rule out sepsis?
No
Empiric treatment for septic arthritis
- if not at risk for STD
- If at risk for STD
- Vancomycin IV plus ceftriaxone IV
2. Nafcillin or ceftriaxone
Causes of gout
Decreased urate excretion (90% of cases)–> renal disease, drugs (cyclosporine, alcohol, nicotinic acid, thiazides etc)
Increased urate production (10%)–> metabolic syndrome (obesity, HTN), increased metabolism (alcohol, hemolytic anemia, psoriasis), neoplastic (MPD, chemo, lymphoproliferative disorder)
Precipitants of gout
Surgery Dehydration Fasting Binge eating Binge drinking Exercise Trauma
What is a test to check for gout
Tap the joint
24 hour urine Uric acid collection
Tophi aspiration
Management of gout
Acutely–> NSAIDs (I.e naproxen), systemic corticosteroids, intra articulate corticosteroids, colchicine during acute attack
Long term–> purine restricted diet (low red meat, low seafood, high low fat dairy products, high fruit and veg), allopurinol
In what conditions would you see a polyarthritis with a temperature above 40
Stills
Bacterial arthritis
SLE
In what conditions would you see a polyarthritis with fever preceding arthritis
Viral arthritis Lyme Reactive arthritis Stills bacterial endocarditis
In what conditions would you see a polyarthritis with migratory arthritis
Rheumatica fever Gonococcemia Meningococcemia SLE Acute leukaemia Whipple's
In what conditions would you see a polyarthritis with morning stiffness
RA
Polymyalgia rheumatica
Stills
In what conditions would you see a polyarthritis with pain disproportionally greater than effusion
Rheumatic fever
Familial Mediterranean fever
Acute leukaemia
AIDS
In what conditions would you see a polyarthritis with effusion disproportionately greater than pain
TB arthritis
Bacterial endocarditis
IBD
Lyme
In what conditions would you see a polyarthritis with symmetrical small joint synovitis
RA
SLE
Viral
In what conditions would you see a polyarthritis with leukopenia
SLE
Viral
In what conditions would you see a polyarthritis with positive RF
RA (sens and spec 70%) Viral arthritis SLE Sarcoidosis Systemic vasculitis
In what conditions would you see a polyarthritis with positive ACPA (anti cyclic cirtullinated peptide antibodies)
RA–not sensitive but highly specific
