Hi

Urinary retention is frequently tested side effect , caused by :

Atropine
TCAs
Antihistamines of first generation...

Causes of urinary retention
These are numerous and can be classified as:[1]

In men - benign prostatic hypertrophy (BPH), meatal stenosis, paraphimosis, penile constricting bands, phimosis, prostate cancer.
In women - prolapse (cystocele, rectocele, uterine), pelvic mass (gynaecological malignancy, uterine fibroid, ovarian cyst), retroverted gravid uterus.
In both - bladder calculi, bladder cancer, faecal impaction, gastrointestinal or retroperitoneal malignancy, urethral strictures, foreign bodies, stones.

Infectious and inflammatory:

In men - balanitis, prostatitis and prostatic abscess.
In women - acute vulvovaginitis, vaginal lichen planus and lichen sclerosis, vaginal pemphigus.
In both - bilharzia, cystitis, herpes simplex virus (particularly primary infection), peri-urethral abscess, varicella-zoster virus.
Drug-related:
Up to 10% AUR episodes are thought to be attributable to drugs. Those known to increase risk include:

Anticholinergics (eg, antipsychotic drugs, antidepressant agents, anticholinergic respiratory agents).
Opioids and anaesthetics.
Alpha-adrenoceptor agonists.
Benzodiazepines.
Non-steroidal anti-inflammatory drugs.
Detrusor relaxants.
Calcium-channel blockers.
Antihistamines.
Alcohol.
Neurological:
More often causing chronic retention but may cause AUR:

Autonomic or peripheral nerve (eg, autonomic neuropathy, diabetes mellitus, Guillain-Barré syndrome, pernicious anaemia, poliomyelitis, radical pelvic surgery, spinal cord trauma, tabes dorsalis).
Brain (eg, cardiovascular disease (CVD), MS, neoplasm, normal pressure hydrocephalus, Parkinson's disease).
Spinal cord (eg, invertebral disc disease, meningomyelocele, MS, spina bifida occulta, spinal cord haematoma or abscess, spinal cord trauma, spinal stenosis, spinovascular disease, transverse myelitis, tumours, cauda equina).
Other:

In men - penile trauma, fracture, or laceration.
In women - postpartum complications (increased risk with instrumental delivery, prolonged labour and Caesarean section),[2]urethral sphincter dysfunction (Fowler's syndrome).
In both - pelvic trauma, iatrogenic, psychogenic.

 

Good work, keep it going, I request all recent test takers to share topics which were asked..

Good luck to everyone..

 

Bacterial Endocarditis

Bacterial endocarditis

Fever most common
Roth's spots on retina
Osler's nodes on fingers
New murmurs
Janeway lesions, on palms or soles
Anemia
Splinter hemorrhages on nail bed
Valvular damage
Can be caused by Staph aureus, as acute form
And caused by viridans streptococci as subacute form

 

Two elements

Bacterial endocarditis

Fever most common
Roth's spots on retina
Osler's nodes on fingers
New murmurs
Janeway lesions, on palms or soles
Anemia
Splinter hemorrhages on nail bed
Valvular damage
Can be caused by Staph aureus, as acute form
And caused by viridans streptococci as subacute form

If you see combination of Fever plus murmur, it should be definetily bacterial endocarditis, watch videos from Dr. Conrad Fisher about Bacterial endocarditis, and if you have time other 20 videos, that will add and make strong knowledge in the last few days before exam...

 

Cranial nerve 4

Vertical diplopia is the most noticeable when the affected eye looks toward the nose, as occurs when reading the NEWSPAPER OR WALKING DOWNSTAIRS...

 

Cavernous Sinus Syndromes

Cavernous Sinus Syndromes

Background
Cavernous sinus syndrome is defined by its resultant signs and symptoms: ophthalmoplegia, chemosis, proptosis, Horner syndrome, or trigeminal sensory loss. Infectious or noninfectious inflammatory, vascular, traumatic, and neoplastic processes are the principal causes. Examples of specific entities that may result in cavernous sinus syndrome are myriad and include carotid artery aneurysms, carotid-cavernous fistulas (C-C fistulas) (see image below), tumors, and Tolosa-Hunt syndrome, to name the most frequently discussed.

Carotid-cavernous fistula.
Carotid-cavernous fistula.
Pathophysiology
The cavernous sinuses are paired, venous structures located on either side of the sella turcica. They receive venous tributaries from the superior and inferior orbital veins and drain into the superior and inferior petrosal sinuses. The cavernous sinus contains the carotid artery, its sympathetic plexus, and the oculomotor nerves (third, fourth, and sixth cranial nerves). In addition, the ophthalmic branch and occasionally the maxillary branch of the fifth nerve traverse the cavernous sinus. The nerves pass through the wall of the sinus while the carotid artery passes through the sinus itself.

Physical
Cavernous sinus lesions are characterized by the following signs:
Unilateral and isolated third, fourth, or sixth cranial nerve palsy
Combination patterns of ophthalmoplegia
Painful ophthalmoplegia
Proptosis (pulsating exophthalmos suggests a direct C-C fistula)
Ocular and cranial bruits
Conjunctival congestion; arterialization of conjunctival veins
Ocular hypertension
Optic disc edema or pallor; retinal hemorrhages
Anesthesia in the ophthalmic division of the trigeminal nerve (V1) and/or decreased or absent corneal reflex and possibly anesthesia in the maxillary or V2 branch
Pupil in midposition and nonreactive if both sympathetics and parasympathetics from the third nerve are affected
Cavernous sinus tumors
Metastatic lesions - Isolated or combined ophthalmoplegia, painful ophthalmoplegia, anesthesia in the ophthalmic nerve
Pituitary tumors - Isolated or combined ophthalmoplegia (lateral extension); endocrine signs such as acromegaly, galactorrhea, and unitemporal or bitemporal visual field defects
Primary intracranial tumors - Isolated or combined ophthalmoplegia and/or primary aberrant regeneration of the third cranial nerve
Cavernous sinus aneurysms
Isolated or combined ophthalmoplegia
Painful ophthalmoplegia
Decreased pain sensation in the V1 ophthalmic division

 

Hi

Air vs. bone conductive hearing loss[edit]
Air conduction uses the apparatus of the ear (pinna, eardrum and ossicles) to amplify and direct the sound whereas bone conduction bypasses some or all of these and allows the sound to be transmitted directly to the inner ear albeit at a reduced volume, or via the bones of the skull to the opposite ear.

Description Relative Positive/negative
In a normal ear, air conduction (AC) is better than bone conduction (BC) AC > BC this is called a positive Rinne

In conductive hearing loss, bone conduction is better than air AC < BC negative Rinne

In sensorineural hearing loss, bone conduction and air conduction are both equally depreciated, maintaining the relative difference of bone and air conductions AC > BC positive Rinne

In sensorineural hearing loss patients there may be a false negative Rinne AC < BC negative Rinne

 

Bell's palsy

Bell's palsy, or cranial nerve VII involvement... LOWER MOTONEURON LESION

Complete destruction of the facial nucleus itself or its branchial efferent fibers

Peripheral ipsilateral facial paralysis with inability to close eye on involved side.

As complication of AIDS,Lyme disease, herpes simplex, sarcoidosis, tumors, diabetes...

Most commonly seen in LYME DISEASE AND SARCOIDOSIS...

 

Hi

Visual field defects

 

Number needed to treat

Number needed to treat

The number needed to treat (NNT) can be thought of as the number of patients that need to be treated in order for one to benefit. It provides an attractive means of summarising the results of a clinical trial in a single figure, because the meaning of a sentence such as '20 patients need to be treated to avoid one additional death over a five year period' is easily understood by both doctors and patients.1

Calculation

The NNT is the inverse of the absolute risk reduction - the difference between the proportion or rate of events in the active treatment intervention group (Pa) and the proportion of events in the control group (Pc):

Number needed to treat =1/(Pa-Pc)

 

Multiple Sclerosis

Multiple Sclerosis

Autoimmune inflammation and demyelination of CNS.
Patients can present with optic neuritis, MLF syndrome, hemiparesis, hemisensory, bladder and bowel incontinence.
Most often affects women in their 20s to 30s.
Findings increased IgG in cerebrospinal fluid.

Periventricular plaques.>>>> areas of oligodendrocyte loss and reactive gliosis.

Classic triad is:
Scanning speech
Intention tremor,
Incontinence..............internuclear ophthalmoplegia , Nystagmus..

 

Tension headache

Tension headache

Consistent, non- throbbing pain ( lasts 4-6 hours up to 7 days)
Occurs in the frontal occipital regions ( most often bilateral)
Or as a band around the head

NO associated symptoms such as: Sensitivity to ligh or noise
vision disturbance
naussea or vomiting
FOcal neurological change

 

Migrane headache

Migrane headache

Most common in women
Al least 5 attacks
Headache lasting 4-72H
At least of the following:
Location>>>>>>>>>>> Unilateral
Quality>>>>>> throbbing, pulsating

Moderate to severe intensity( inhibits or prohibits daily activity)
Aggravated by routine physical activity
At least one of the following:
Nausea , vomiting
Photophobia or and phonophobia.

25% have AURA before

 

Cluster headache

Cluster headache

Strictly unilateral

Severe piercing, boring pain in the retroorbital, periorbital region
Does not throb like a migrane. No aura
Duration from 15 minutes to 3 hours, occurs daily
Often at the same time, i name this headache punctual and disciplinary and continues for an interval of 4-8 weeks
May be associated with partial Horner syndrometosis , myosis, anhydrosis.

Ipsilateral eye redness, tearing, rhinorrhea or nasal congestion

 

Tuberous sclerosis

Tuberous sclerosis

Hamartomas in CNS and skin,
Adenoma sebaceum( cutaneous angiofibromas)
Mitral valve regurgitation
Ash-leaf spots
Cardiac Rhabdomyoma (Tuberous sclerosis)
Autosomal dominant
Mental retardation
Renal Andiomyolipoma
Seizures
Shagreen patches
Increased incidence of subependymal astrocytomas ungual fibromas

 

Glioblastoma multiforme

Glioblastoma multiforme

Most common primary brain tumor.
Prognosis grave, less than one year expectancy. FOund in cerebral hemispheres.
Can cross corpus callosum and create a image like Butterfly glioma
Stain astrocytes for GFAP (Glial fibrillary acidic protein)

Pseudopalisading key word ,pleomorphic tumor cells, border central areas of necrosis and hemorrhage. Derived from glial cells

 

Pylocytic astrocytoma

Pylocytic astrocytoma

most common brain tumor in children
Usualy well circumscribed. found in posterior fossa.
May be supratentorial.
We know that majority of childhood tumors are infratentorial
GFAP positive.
Benign with a good prognosis

Rosenthal fibers- eosinophilic, corkscrew fibers.
Cystic plus solid (gross)
Arises in the cerebellum

 

Medulloblastoma

Medulloblastoma

Second most common brain tumor in children
Highly malignant cerebellar tumor
A form of primitive neuroectodermal tumor PNET
Can compress 4th ventricle , causing HYDROCEPHALUS.
Sheets of small cells with deeply basophilic nuclei, and scant cytoplasm

Rosettes or perivascular pseudorosette pattern of cells. Solid( gros). small blue cells histology

Cerebelar vermis is the most common location of a medulloblastoma symptoms include signs of increased intracranial pressure like morning headache, vomiting, lethargy,. Cerebelar dysfunction occurs as the tumor compresses adjacent structures.

 

Phenytoin

Phenytoin

Not as important as mechanism of action of clinical use as adverse effects

Use dependent blockade of Na+ channels, increase refractory period,
Inhibition of glutamate release which is excitatory neurotransmitter,

Clinical use: tonic clonic seizures. also a class IB antiarrhythmic

Toxicity :Nystagmus , ataxia, diplopia, sedation, SLE like syndrome, induction of P450, Chronic use produces gingival hyperplasia in children, peripheral neuropathy, hirsutism, megaloblastic anemia because decrease folate absorption. Teratogenic, as fetal hidantoin syndrome causes.

Concisely :
Gingival hyperplasia
Hirsutism
Fetal hydantoin syndrome
Induces P450
Stevens-Johnson syndrome
Drug induced lupus

Fetal Hydantoin Syndrome is a rare disorder that is caused by exposure of a fetus to the anticonvulsant drug phenytoin (Dilantin). The symptoms of this disorder may include abnormalities of the skull and facial features, growth deficiencies, underdeveloped nails of the fingers and toes, and/or mild developmental delays. Other findings occasionally associated with this syndrome include cleft lip and palate, having an unusually small head (microcephaly) and brain malformations with more significant developmental delays.

 

Neroleptic malignang syndrome

Neuroleptic malignant syndrome

Increased body temperature >38°C (>100.4°F), or
Confused or altered consciousness
Diaphoresis "sweat shock"
Rigid muscles
Autonomic imbalance

Differential diagnosis with :
encephalitis, toxic encephalopathy, status epilepticus, heat stroke, and malignant hyperthermia

Causes
NMS is usually caused by antipsychotic drug use, and a wide range of drugs can result in NMS.[1] Individuals using butyrophenones (such as haloperidol and droperidol) or phenothiazines (such as promethazine and chlorpromazine) are reported to be at greatest risk. However, various atypical antipsychotics such as clozapine, olanzapine, risperidone, quetiapine, and ziprasidone have also been implicated in cases.[10]

NMS may also occur in people taking dopaminergic drugs (such as levodopa) for Parkinson's disease, most often when the drug dosage is abruptly reduced.[11] In addition, other drugs with anti-dopaminergic activity, such as the antiemetic metoclopramide, can induce NMS.[12] Even drugs without known anti-dopaminergic activity have been associated with NMS; examples include amoxapines and lithium. Also, desipramine, dothiepin, phenelzine, tetrabenazine, and reserpine have been known to trigger NMS.[13] At the molecular level, NMS is caused by a sudden, marked reduction in dopamine activity, either from withdrawal of dopaminergic agents or from blockade of dopamine receptors.

The mechanism is thought to depend on decreased levels of dopamine activity due to:

Dopamine receptor blockade
Genetically reduced function of dopamine receptor D2

Pathophisiology

The most widely accepted mechanism by which antipsychotics cause neuroleptic malignant syndrome is that of dopamine D2 receptor antagonism. In this widely accepted model, central D2 receptor blockade in the hypothalamus, nigrostriatal pathways, and spinal cord leads to increased muscle rigidity and tremor via extrapyramidal pathways. Hypothalamic D2 receptor blockade results in an elevated temperature set point and impairment of heat-dissipating mechanisms. Peripherally, antipsychotics lead to increased calcium release from the sarcoplasmic reticulum, resulting in increased contractility, which can contribute to hyperthermia, rigidity, and muscle cell breakdown.

Beyond these direct effects, D2 receptor blockade might cause neuroleptic malignant syndrome by removing tonic inhibition from the sympathetic nervous system. The resulting sympathoadrenal hyperactivity and dysregulation leads to autonomic dysfunction. This model suggests that patients with baseline high levels of sympathoadrenal activity might be at increased risk. While this has not been proven in controlled studies, several such states have been proposed as risk factors for neuroleptic malignant syndrome.[5]

Direct muscle toxicity also has been proposed as a mechanism of neuroleptic malignant syndrome.

NMS is a medical emergency

Treatment:

stop the antipsychotic medication and treat the hyperthermia aggressively

Dantrolene has been used when needed to reduce muscle rigidity

Amantadine is another treatment option due to its dopaminergic and anticholinergic effects

Benzodiazepines may be used to control agitation

more recently dopamine pathway medications such as bromocriptine

 

Malignant hyperthermia

Malignant hyperthermia

Susceptibility to MH is often inherited as an autosomal dominant disorder, for which there are at least 6 genetic loci of interest,[2] most prominently the ryanodine receptor gene (RYR1). MH susceptibility is phenotypically and genetically related to central core disease (CCD), an autosomal dominant disorder characterized both by MH symptoms and myopathy

Symptoms

The typical symptoms of malignant hyperthermia are due to a hypercatabolic state, which presents as a very high temperature, an increased heart rate and breathing rate, increased carbon dioxide production, increased oxygen consumption, acidosis, rigid muscles, and rhabdomyolysis

Causes
Volatile anesthetics,
And single depolarizing muscle blocker Succinylcholine

Treatment
dantrolene

 

Mesothelioma

Mesothelioma


Mesothelioma is a malignant neoplasm arising from mesothelial cells.
Body cavities ( pleural, peritoneal, pericardial) are lined with mesothelium.
Asbestos exposure is the only significant risk factor
Individuals involved in asbestos mininm and industrial application of asbestos like insulation and shipbuilding

The symptoms of mesothelioma include DISPNEA AND CHEST PAIN
Hemorrhagic pleural infusion are frequently present.
Nodular or smooth pleural thickening is the main finding on Roentgen

 

Hi

Formulas from Renal physiology

Cx=UxV/P
Where Ux is urine concentration of X
V urine flow rate
Px plasma concentration of X

FF=GFR/RPF
Glomerular Filtration Rate, may use inulin because is freely filtered and aproximate with 100-120 mL/min

Renal plasma flow , may be used Paraaminohypuric because is both filtered and actively secreted.

RBF=RPF/ (1-hematocrit)

 

Lateral medullary syndrome

Lateral medullary syndrome (also called Wallenberg syndrome and posterior inferior cerebellar artery syndrome) is a disorder in which the patient has a constellation of neurologic symptoms due to injury to the lateral part of the medulla in the brain, resulting in tissue ischemia and necrosis.

Signs and symptoms
This syndrome is characterized by sensory deficits affecting the trunk (torso) and extremities on the opposite side of the infarction and sensory deficits affecting the face and cranial nerves on the same side with the infarct. Specifically, there is a loss of pain and temperature sensation on the contralateral (opposite) side of the body and ipsilateral (same) side of the face. This crossed finding is diagnostic for the syndrome.

Clinical symptoms include swallowing difficulty, or dysphagia slurred speech, ataxia, facial pain, vertigo, nystagmus, Horner's syndrome, diplopia, and possibly palatal myoclonus.

Weber's syndrome

Weber's syndrome (superior alternating hemiplegia) is a form of stroke characterized by the presence of an oculomotor nerve palsy and contralateral hemiparesis or hemiplegia

 

Acute poststreptococcal glomerulonephritis

Acute poststreptococcal glomerulonephritis

on LM>>>> glomeruli enlarged and hypercellular, neutrophils, LUMPY_BUMPY appearance
on EM >>>> subepithelial immune complex humps
on IF>>>> granular appearance due to IgG, IgM, C3 deposition along th GBM and mesangium

Most frequently seen in children. Peripheral and periorbital edema and dark urine.
Resolves spontaneously.

Decreased level of C3

M protein define nephritogenic strains...

 

Focal segmental glomerulonephritis

Focal segmental glomerulonephritis

Most common in adults

on LM segmental sclerosis and hyalinosis
Most common glomerular disease in HIV, Heroin use, sickle cell disease