Most Common Site of Primary Bone Tumors
- Chondroblastoma (before physeal closure)
- Osteoclastom/Giant cell tumor (after physeal closure in adults)
- Articular osteochondroma
- Bone cyst
- Osteoclastoma (in children)
- Osteomyelitis mostly starts in metaphysis
- Round cell lesions: Ewing’s sarcoma/Multiple myeloma /Reticulum cell sarcoma
- Osteoid osteoma
Inguinal area (over inguinal canal).
Anterior and Lateral part of Upper 2/3rdof thigh.
Anterior, Lateral & Medial part of Lower 1I3'd of thigh and knee.
Medial side of leg.
Lateral side of leg, Medial half of dorsum of foot, first web space.
Posterior surface of ankle, and lateral half of dorsum of foot.
Posterior of thigh and leg.
Gluteal area around perianal region, Groin.
Perianal skin &Groin.
1. Hypothermia → Elevation of the j-point — Osborne wave.
2. Hyperkalemia → peaking (tenting) of T-wave, ↓-P-wave amplitude, widening of the QRS interval, cardiac arrest with sine wave (in severe Hyper kalemia)
3. Hypokalemia → Prominent ‘U’-wave, prolongation of ‘QT’ interval.
4. Hypocalcemia → Prolong QT interval
5. Hyper calcemia — Short QT interval.
6. Digitalis toxicity — short QT interval with “scooping” of the ST-T wave comples (i.e. Depression of ST-T segment)
7. Sub arachnoid Hemorrhage→ “CVAT-wave” pattern → marked QT prolongation with deep wide T-wave inversions
8. M.I → T-wave inversion
Catecholamines Agonists :
A and B receptors - B1, A1, B2
- Good for emergency bronchospasm treatment (acute asthma or anaphylactic shock) and open-angle glaucoma
- Also gives longer duration of anesthetic action via vasocontriction and reducing systemic absorption
- Increases sBP lowers dBP
- A and B in therapeutic doses, most A receptor influence
- Good to increase peripheral resistance (A1)
- Good for shock treatment (increase TPR and BP); increases sBP and dBP
- Synthetic: B1 and B2, little A stimulation
- Strong cardiac stimulation (b1), dilation of skeletal vessels (b2), and bronchodilation (b2)
- Increases sBP lowers dBP
- Precursor to NE; A and B activity and dopamine receptors in renal and mesenteric vasculature causing vasodilation
- B1 stimulation of the heart
- Therapeutic: choice drug for shock as it increases BP via cardiac stimulation and also increases kidney blood flow (increased GFR and Na diuresis)
- Synthetic B1 agonist
- To increase CO in CHF
- Watch out in Afib as it may increase AV conduction
Phenylephrine - Synthetic A1 agonist – for nasal decongestion
Methoxamine - Synthetic A1 agonist – for hTN in surgery
Clonidine - A2 agonist- - Used to lower pressure in essential HTN (via CNS effect, diminishing sympathetic outflow)
Common pathogens attributed to food poisoning include Norovirus, Salmonella, Clostridium perfringens, Campylobacter jejuni, Staphylococcus aureus, and Escherichia coli.
Incubation periods depend on the cause, and range from a few hours to days. The clinical presentation associated with food poisoning varies, but typical symptoms include diarrhea, nausea, vomiting, and abdominal cramping.
Staphylococcal food poisoning
Pathogen: Staphylococcus aureus
Some strains produce heat-stable enterotoxins that cause staphylococcal food poisoning.
Transmission: ingestion of preformed toxins in contaminated food
Typically involves a short latency period; resolution of symptoms after 24–48 hours
Bacteria proliferate in inadequately refrigerated food (canned meats, mayonnaise/potato salad, custards).
Incubation period: 1–4 hours
Clinical findings: nausea, vomiting, abdominal discomfort, diarrhea
Bacillus cereus infection
Pathogen: Bacillus cereus, a heat-stable, spore-forming bacterium that produces two different enterotoxins
Transmission: The bacterium grows in heated food that cools down too slowly or is improperly refrigerated. Reheated rice is a common source of infection.
Incubation period and clinical findings
Enterotoxin I (emetic form): 30 min to 6 h after ingestion → nausea and vomiting
Enterotoxin II (diarrheal form): 6–15 h after ingestion → watery diarrhea for 24–48 h
Food poisoning from reheated rice - (B. cereus).
Management of H. Pylori Infection
- Gram – rod
- Causes erosion of protective epithelial cells -> gastritis or peptic ulcer
H2 antagonist or PPI + Abx
- Metronidazole or amoxicillin/clarithromycin
- PPI + 2 or 3 antimicrobials is standard
- Ex: Ranitidine + Peptobismol + Clarithromycin + Amoxicillin 7-14 days
-Add bismuth if resistant H. pylori
- Ex: PPI + BMT (Bismuth + Metronidazole + tetracycline) 7days
Treatment for ZE Syndrome
- Gastrinoma of the duodenum or pancreas
-Elevated gastrin levels- Peptic/gastric ulcers
High dose PPI until resorting to surgery or chemotherapy for tumor removal
- Works on Cyclo-oxygenase (AA -> thromboxane)
- Low dose (80-160 mg/day) irreversibly inhibits plt COX, and they can’t make new COX b/c they have no nucleus
- Some inhibition of endothelial COX but not much, therefore prostacyclin (anti-coag) synthesis isn’t affected much
- Benefit is greater after thrombolysis
- SE is bleeding
- Prophylaxis for MI or TIA (80mg/day), higher doses for post-MI/TIA (160-325mg/day)
- Contraindications (bleeding risk): Vit. K def., Hemophilia, Hypoprothombinemia, pregnancy & childbirth
- ADP antagonist
- Competes with ADP for P2Y receptor (prevents lowering of cAMP)
- Less incidence of neutropenia/thrombocytopenia
- Used in combo with ASA
- ADP antagonist, prodrug
- Often used in combo with ASA (synergistic)
- May cause severe neutropenia (1%)
- phosphodiesterase inhibitor (prevents cAMP breakdown)
- Eptifibatide, Abciximab, Tirofiban
- Block the receptor for fibrinogen blocking plt Aggregation
Heparin (& derivatives)
- Stimulates natural anticoags (antithrombin)
- Monitor using aPTT (add negative charges)
- Negatively charged, therefore cannot cross membranes (given IM, IV, parentally)
- Good for pregnancy
- Eliminated by RES & macrophages
- Potentiates AT III (in the plasma) – inhibits IIa, Xa, IXa and VIIa
- Toxicity – hemorrhage
- Antidote – protamine sulfate (1mg for every 100 units of heparin)
Heparin-Induced Thrombocytopenia (HIT) – occurs 5-10 days after, stop heparin immediately; use alternatives lepirudin/danaparoid
- Good for PE and DVT and during pregnancy
LMWH – better bioavailability, can be given subcut. w/o lab monitoring as outpatient, less risk of bleeding
- More expensive, not good in renal failure, not for pregnancy
- DOES NOT inhibit IIa (but inhibit Xa)
- Good for DVT, PE and UA
Danaparoid – promotes inhibition of Xa by AT (for HIT)
Lepirudin – direct thrombin inhibitor (for HIT)
Coumarin (Oral) anticoags
- Monitored using PT (add tissue factor)
- Inhibit Vit. K Epoxide reductase in liver
-Prevents carboxylation of Vit.K dependent factors
-Takes 4-5 days to get effective (carboxylated fx’s in plasma need to be cleared before inactive ones take over)
-Small volume of distribution, steep dose-response curve (small therapeutic window)
- For DVT and PE, prosthetic heart valves or Afib, MI
-Metabolized by CYP1A and CYP2C9
-Efficacy measured by INR, pt’s PT time divided by PT time in pooled plasma
- INR = (PTpt/PTref)^ISI (target is 2.0 – 3.0)
- Warfarin overdose
- Give Excess Vit.K, goes through a diff enzyme that isn’t inhibited by warfarin (Diaphorase)
Fibrinolytics (lyse formed thrombi)
Streptokinase – turns plasminogen -> plasmin
-Plasmin breaks down fibrin (lysis of formed clot) Dissolves clots post-MI/DVT/PE
- SE – bleeding (systemic plasminogen activation), allergy, hTN, fever
- Streptokinase has an additive effect with ASA
Tissue plasminogen activator (tPA) – acts on fibrin and circulating plasminogen -> plasmin
- Less systemic plasmin
- Same indications as streptokinase
- More expensive
Important parasympathetic ganglia in head and neck are :
(i) otic ganglion,
(ii) submandibular ganglion,
(iii) pterygopalatine ganglion
(iv) ciliary ganglion.
Topographically, it is connected to mandibular nerve, while functionally it is related to glossopharyngeal (IX) nerve. Its roots are:-
Sensory root:-By Auriculotemporal nerve.
Sympathetic root:-By sympathetic plexus around middle meningeal artery.
Parasympathetic (secretomotor) root: - This root is by lesser petrosal nerve. Preganglionic fibres begin in inferior salivatory nucleus, pass through glossopharyngeal nerve, then its tympanic branch, tympanic plexus, and the lesser petrosal nerve and relay in otic ganglion.
Postganglionic fibers pass through auriculotemporal nerve and supplies parotid gland.
Motor root :- It is derived from nerve to medial pterygoid which passes unrelayed through ganglion and supplied tensor veli palatini and tensor tympani (Note :- Otic ganglion has a motor root, beside three standard roots of parasympathetic ganglion of head and neck: sensory, sympathetic and parasympathetic).
Functionally, submandibular ganglion is connected to facial nerve, while topographically it is connected to lingual branch ofmandibular nerve. Its roots are :-
Sensory root: - It is from lingual nerve.
Sympathetic root: - It is from sympathetic plexus around facial artery, which contains postganglionic fibers from superior cervical ganglion of sympathetic trunk.
Secretomotor (parasympathetic) root: - Preganglionic fibers arise from superior salivatory nucleus pass through facial nerve then its chorda tympani branch which joins lingual nerve and relay in submandibular ganglion.
Postganglionic fibers supply :-Directly submandibulargland.
Through lingual nerveSublingual salivary gland and glands in oral cavity.
Pterygopalatine Ganglion (Sphenopalatine Ganglion)
It is the largest parasympathetic ganglion, suspended by two roots to maxillary nerve. Functionally, it is related to facial nerve. It is called ganglion of "hay fever". Its roots are:-
Sensory root:-It is from maxillary nerve.
Sympathetic root:-It is sympathetic plexus around internal carotid artery through deep petrosal nerve.
Secretomotor (parasympathetic) root:-Preganglionic fibers arise from lacrimatory nucleus, pass through facial nerve, then to its greater petrosal branch. Greater petrosal nerve unites with deep petrosal nerve (sympathetic fibers) to form nerve to pterygoid canal (Vidian nerve). Fibers reach to pterygopalatine ganglion; only fibers of greater petrosal nerve relay in the ganglion, not of deep petrosal nerve.
Postganglionic fibers supply lacrimal gland and palatal glands, and pharyngeal glands.
Branches of the pterygopalatine ganglion are :-
For lacrimal gland: - Postganglionic fibers pass through zygomatic nerve (branch of maxillary nerve), its zygomaticotemporal division which gives communicating branch to lacrimal nerve for supplying lacrimal gland.
Nasopalatine nerve:-For nasal and palatal glands.
Nasal branches: - For mucous membrane and glands oflateral wall of nasal cavity.
Palatine branches: - One greater palatine and 2-3 lesser palatine branches for glands of soft palate and hard palate.
Orbital branches: - For orbital periosteum.
Pharyngeal branches:-For glands of pharynx.
Topographically, ciliary ganglion is related to nasociliary nerve (a branch of ophthalmic division of trigeminal nerve), but functionally it is related to oculomotor nerve. Its roots are:-
Sensory root:-It is from nasociliary nerve.
Sympathetic root: - It is from plexus around ophthalmic artery.
Parasympathetic root: - It is from a branch to inferior oblique muscle. These fibers arise from Edinger – Westphalnucleus, join oculomotor nerve and then to its branch to inferior oblique to relay in ciliary ganglion.
Postganglionic fibers pass through short ciliary nerves to supply sphincter pupillae and ciliary muscles.
Types of Haemorrhage
Hemorrhaging is broken down into four classes
Class I Hemorrhage involves up to 15% of blood volume.
There is typically no change in vital signs and fluid resuscitation is not usually necessary.
Class II Hemorrhage involves 15-30% of total blood volume.
A patient is often tachycardic (rapid heart beat) with a reduction in the difference between the systolic and diastolic blood pressures.
The body attempts to compensate with peripheral vasoconstriction. Skin may start to look pale and be cool to the touch.
The patient may exhibit slight changes in behavior.
Volume resuscitation with crystalloids (Saline solution or Lactated Ringer's solution) is all that is typically required. Blood transfusion is not usually required.
Class III Hemorrhage involves loss of 30-40% of circulating blood volume.
The patient's blood pressure drops, the heart rate increases, peripheral hypoperfusion (shock) with diminished capillary refill occurs, and the mental status worsens.
Fluid resuscitation with crystalloid and blood transfusion are usually necessary.
Class IV Hemorrhage involves loss of >40% of circulating blood volume.
The limit of the body's compensation is reached and aggressive resuscitation is required to prevent death.
Source of Haemorrhage
- Extra dural haemorrhage - middle meningeal artery
- Sub dural haemorrhage - bridging or diploic veins
- Sub arachnoid haemorrhage - rupture on berry aneursym
- Tennis bal injury to eye - circulis iridis major
- Epistaxis - Sphenopalantine artery
- During tonsillectomy - para tonsilaar veins, tonsilar and ascending palantine artery
- Tracheostomy - isthemus and inferior thyroid vein
- Heamoptysis-bronchial artery
- Gastric ulcer- left gastric, splenic artery
- Duodenal ulcer - gastroduodenal artery
- Hemmorrhoids - submucous rectal venous plexus formed by superior rectal vein & inferior rectal vein
- Retropubic proastatectomy - dorsal venous plexus
- Hysterectomy - internal illac artery
- Menstruation - spiral arteries
- Abnormal synchronous APs of groups of neurons in various parts of brain
- Many casues (infection, fever, tumors, injury, lyte imbalance, etc)
- Therapy aimed to reduce excitability of neurons
Benzodiazepines (Clonazepam, Diazepam) - Diazepam used for status epilepticus
Barbiturates (Phenobarbital)- Benzos and Barbituates increase GABA channel - hyperpolarization of neurons
Gabapentin - Increases gaba release
Valproic acid - Increases GABA, also blocks Na+ and Ca2+ channels, and increase K+ conductance
2.Alter transmembrane flow of ions
Phenytoin- Blocks Na+ channels
Carbamazepine - Blocks Na+ channels and potentiates postsynaptic effect of GABA
Ethosuximde - Blocks Ca2+ channels
Iamotrigine - Blocks Na+ channels
3. Decrease glutamate excitatory tone
Glutamate antagonists have too many side effects and none are on the market as anticonvulstants yet