In the hand, the median nerve supplies the lateral two lumbricals, opponens pollicis, abductor pollicis brevis, and flexor pollicis brevis; the remainder are served by the ulnar nerve.
Wasting of the interossei (prominent guttering of the back of the hand), of the web space between thumb and index finger, and softening and flattening of the hypothenar eminence with sparing of abductor pollicis brevis indicates an ulnar nerve lesion.
Isolated wasting of abductor pollicis brevis indicate median nerve lesion in carpal tunnel syndrome.
Global wasting of hand indicate median and ulnar nerve lesion; probably, with damage to T1 root.
More extensive arm wasting may indicate any of the following: syringomyelia of MND; bilateral, symmetrical wasting indicate peripheral neuropathy.
π₯ #notes
#hand_examination
#plastic_surgery
#orthopedics
#neurosurgery
Wasting of the interossei (prominent guttering of the back of the hand), of the web space between thumb and index finger, and softening and flattening of the hypothenar eminence with sparing of abductor pollicis brevis indicates an ulnar nerve lesion.
Isolated wasting of abductor pollicis brevis indicate median nerve lesion in carpal tunnel syndrome.
Global wasting of hand indicate median and ulnar nerve lesion; probably, with damage to T1 root.
More extensive arm wasting may indicate any of the following: syringomyelia of MND; bilateral, symmetrical wasting indicate peripheral neuropathy.
π₯ #notes
#hand_examination
#plastic_surgery
#orthopedics
#neurosurgery
congenital drenal hyperplasia CAH #pediatrics #endocrinology
#Gynecology
#Ultrasonography
Obstruction within the distal vagina is usually responsible for the development of a #hematocolpos.
If there is a backup of blood or fluid in the vagina, this may extend into the uterine cavity & result in an associated #hematometra.
#imperforate_hymen
#transverse_vaginal_septum
#cervical_agenesis
#Ultrasonography
Obstruction within the distal vagina is usually responsible for the development of a #hematocolpos.
If there is a backup of blood or fluid in the vagina, this may extend into the uterine cavity & result in an associated #hematometra.
#imperforate_hymen
#transverse_vaginal_septum
#cervical_agenesis
π§ Medical Studentsβ’ π§
https://youtu.be/SEQPKTceWp4 #obstetrics #PPH
Management of PPH during C/S.
#obstetrics
#obstetrics
π§ Medical Studentsβ’ π§
https://youtu.be/SEQPKTceWp4 #obstetrics #PPH
Management of PPH after vaginal delivery.
#obstetrics
#obstetrics
Couvelaire uterus (also known as uteroplacental apoplexy) is a life-threatening condition in which loosening of the placenta (abruptio placentae) causes bleeding that penetrates into the uterine myometrium forcing its way into the peritoneal cavity.
#obstetrics & #gynecolgy
#obstetrics & #gynecolgy
Forwarded from Medical Mnemonics
π§© Medical Mnemonics
Immediate Treatment of Acute
ππ΄ BEMOAN
γ½Ξ²-blocker
γ½Enoxaparin
γ½Morphine
γ½Oxygen
γ½ASA
γ½Nitroglycerin
ββββββββββββββββ
Alternatively in detail;
π€ OBESE MAN ππ±π
π₯©Oxygen
π₯©Beta blocker
π₯©Statin
π₯©Enoxaparin
π₯©Morphine
π₯©Aspirin
+ ACE-Inhibitor
π₯©Nitrates
#cardiology
γ°γ°γ°γ°γ°γ°γ°γ°γ°γ°γ°
Β©Medical Mnemonics
Immediate Treatment of Acute
MIππ΄ BEMOAN
γ½Ξ²-blocker
γ½Enoxaparin
γ½Morphine
γ½Oxygen
γ½ASA
γ½Nitroglycerin
ββββββββββββββββ
Alternatively in detail;
π€ OBESE MAN ππ±π
π₯©Oxygen
π₯©Beta blocker
π₯©Statin
π₯©Enoxaparin
π₯©Morphine
π₯©Aspirin
+ ACE-Inhibitor
π₯©Nitrates
#cardiology
γ°γ°γ°γ°γ°γ°γ°γ°γ°γ°γ°
Β©Medical Mnemonics
#Cardiology
#Medicine
Heart Failure π₯΄π
Definition: is a condition in which the heart is unable to pump sufficient amount of blood to maintain blood flow to meet the body's demand.
-Mild to moderate degree be symptomatic during exercise.
-Sever degree symptomatic even during test.
Some classifications of heart failure:
1-according to pathophysiology :High ,low (COP) heart failure.
2-according to clinical presentation (signs,symptoms):left,right,biventricular heart failure.
3-according to management or onset :acute ,chronic heart failure.
βοΈ [According to pathophysiological classification:]
Notes:
COP=Stroke volumeΓHeart rate
SV=End diastolic volume -End systolic volume
EDV:called preload,the volume and pressure of blood in ventricles at the end of diastole (dilation),so is the capacity of stretching.
ESV:called afterload,the volume and pressure of blood in ventricles during systole.
So is the force of contraction .
According to starling law: Force of contraction related directly to Capacity of stretching,
So when there is increase in preload ,there is related increasing in afterload .
Contractility:is intrinsic ability of myocardium for forceful contraction at given fiber length.
βοΈSV depends on:
1-preload
2-afterload
3-contractility
β¨any defect in these mechanisms lead to heart failure.
A-Low COP heart failure:
causes:
1-increase of preload,chronic volume overload:
-aortic ,mitral valves regurgitation (Lt HF).
-VSD,ASD (Right HF).
2-decrease of preload(inflow obstruction) :mitral,tricuspid valves stenosis.
3-increase of afterload (outflow obstruction):
-hypertension, aortic valve stenosis (Lt HF).
-Pulmonary hypertension, pulmonary valve stenosis (Rt HF).
-diastolic dysfunction: constrictive pericarditis, restrictive cardiomyopathy, cardiac lemonade.
4-decrease contractility :
-MI.
-Myocarditis.
-Cardiomyopathies
5-arrythmias: Atrial fibrillation, CHB, tachycardia
Mechanisms:
1-hypertrophy of smooth muscle lead to obstruct the flow of coronary arteries lead to ischemia and necrosis and increase of demand.
2-decrease the preload lead to decrease the afterload.
3-decrease the contractility .
4-tachycardia leads to fatigue of myocardium and decrease filling time,
bradycardia ,decrease the contractility leads to heart failure even SV is normal.
B-High COP heart failure:
In condition that the body gets a hyper dynamic circulation:
1-Thyrotoxicosis.
2-Chronic sever anemia.
3-Beri-beri syndrome.
4-Pagetβs disease of bone.
5-AV fistula.
In high COP HF the pulse rate may be wide >60mmgh.
Note: Compensatory mechanism of body to activate RAAS,SNS in low COP lead to increase load on myocardium end by hypertrophy and ischemia.
βοΈ[According to clinical presentation:]
1-left side HF:
Causes:
[systemic HTN, valvular heart diseases,MI,CAD,AF,drugs or alcohol,myocarditis,cardiomyopathy,immune disorder]
Presentation:
-pulmonary edema (crackles).
-hypoxia (SaPo2<90%).
-tachypnea.
-SOB.
-displaced Apex beat.
*cardiac asthma may occurs.
2-Right side HF:
Causes: chronic lung disease(cor-pulmonale), pulmonary hypertension, pulmonary valve stenosis, ASD, VSD, myocarditis, cardiomyopathy.
Presentation:
-peripheral Odem.
-ascites.
-elevated JVP.
-hepatosplenomegaly.
-ventricular heaven.
#Medicine
Heart Failure π₯΄π
Definition: is a condition in which the heart is unable to pump sufficient amount of blood to maintain blood flow to meet the body's demand.
-Mild to moderate degree be symptomatic during exercise.
-Sever degree symptomatic even during test.
Some classifications of heart failure:
1-according to pathophysiology :High ,low (COP) heart failure.
2-according to clinical presentation (signs,symptoms):left,right,biventricular heart failure.
3-according to management or onset :acute ,chronic heart failure.
βοΈ [According to pathophysiological classification:]
Notes:
COP=Stroke volumeΓHeart rate
SV=End diastolic volume -End systolic volume
EDV:called preload,the volume and pressure of blood in ventricles at the end of diastole (dilation),so is the capacity of stretching.
ESV:called afterload,the volume and pressure of blood in ventricles during systole.
So is the force of contraction .
According to starling law: Force of contraction related directly to Capacity of stretching,
So when there is increase in preload ,there is related increasing in afterload .
Contractility:is intrinsic ability of myocardium for forceful contraction at given fiber length.
βοΈSV depends on:
1-preload
2-afterload
3-contractility
β¨any defect in these mechanisms lead to heart failure.
A-Low COP heart failure:
causes:
1-increase of preload,chronic volume overload:
-aortic ,mitral valves regurgitation (Lt HF).
-VSD,ASD (Right HF).
2-decrease of preload(inflow obstruction) :mitral,tricuspid valves stenosis.
3-increase of afterload (outflow obstruction):
-hypertension, aortic valve stenosis (Lt HF).
-Pulmonary hypertension, pulmonary valve stenosis (Rt HF).
-diastolic dysfunction: constrictive pericarditis, restrictive cardiomyopathy, cardiac lemonade.
4-decrease contractility :
-MI.
-Myocarditis.
-Cardiomyopathies
5-arrythmias: Atrial fibrillation, CHB, tachycardia
Mechanisms:
1-hypertrophy of smooth muscle lead to obstruct the flow of coronary arteries lead to ischemia and necrosis and increase of demand.
2-decrease the preload lead to decrease the afterload.
3-decrease the contractility .
4-tachycardia leads to fatigue of myocardium and decrease filling time,
bradycardia ,decrease the contractility leads to heart failure even SV is normal.
B-High COP heart failure:
In condition that the body gets a hyper dynamic circulation:
1-Thyrotoxicosis.
2-Chronic sever anemia.
3-Beri-beri syndrome.
4-Pagetβs disease of bone.
5-AV fistula.
In high COP HF the pulse rate may be wide >60mmgh.
Note: Compensatory mechanism of body to activate RAAS,SNS in low COP lead to increase load on myocardium end by hypertrophy and ischemia.
βοΈ[According to clinical presentation:]
1-left side HF:
Causes:
[systemic HTN, valvular heart diseases,MI,CAD,AF,drugs or alcohol,myocarditis,cardiomyopathy,immune disorder]
Presentation:
-pulmonary edema (crackles).
-hypoxia (SaPo2<90%).
-tachypnea.
-SOB.
-displaced Apex beat.
*cardiac asthma may occurs.
2-Right side HF:
Causes: chronic lung disease(cor-pulmonale), pulmonary hypertension, pulmonary valve stenosis, ASD, VSD, myocarditis, cardiomyopathy.
Presentation:
-peripheral Odem.
-ascites.
-elevated JVP.
-hepatosplenomegaly.
-ventricular heaven.
π1
Forwarded from last Medical Mnemonics
Hemochromatosis Clinical features:
A B C D (h)
πArthralgia
πBronze skin
πCardiomyopathy, Cirrhosis Of liver
πDiabetes (pancreatic damage)
πhypogonadism (anterior pituitary damage)
Follow For Daily Medical Mnemonicsππ@lastmedicalmnemonics
A B C D (h)
πArthralgia
πBronze skin
πCardiomyopathy, Cirrhosis Of liver
πDiabetes (pancreatic damage)
πhypogonadism (anterior pituitary damage)
Follow For Daily Medical Mnemonicsππ@lastmedicalmnemonics
Forwarded from last Medical Mnemonics
SWELLINGS WHICH APPEAR AND DISAPPEAR:
C H I P
π Choledochal Cyst
π Hydronephrosis
π Intussusception
π Pancreatic pseudocyst
C H I P
π Choledochal Cyst
π Hydronephrosis
π Intussusception
π Pancreatic pseudocyst
Thyroid Ophthalmopathy: is an autoimmune inflammatory disorder of the orbit and periorbital tissues, characterized by upper eyelid retraction, lid lag, swelling, redness (erythema), conjunctivitis, and bulging eyes (exophthalmos).
Dermopathy: localized thickening of the skin commonly seen in the pretibial area.
and Acropachy: means thickening of the extremities and it is manifested by a triad of signs: digital clubbing, soft tissue swelling of the hands and feet, and periosteal new bone formation.
specific signs of Grave's disease
#Hyperthyroidism
#Endocrinology
#Medicine
Dermopathy: localized thickening of the skin commonly seen in the pretibial area.
and Acropachy: means thickening of the extremities and it is manifested by a triad of signs: digital clubbing, soft tissue swelling of the hands and feet, and periosteal new bone formation.
specific signs of Grave's disease
#Hyperthyroidism
#Endocrinology
#Medicine
π§ Medical Studentsβ’ π§
Thyroid Ophthalmopathy: is an autoimmune inflammatory disorder of the orbit and periorbital tissues, characterized by upper eyelid retraction, lid lag, swelling, redness (erythema), conjunctivitis, and bulging eyes (exophthalmos). Dermopathy: localized thickeningβ¦
#clinical_case_scenario
A 56-year-old man was referred to a dermatologist for assessment of the progression of his thyroid dermopathy. Three years earlier he had received a diagnosis of Gravesβ disease with thyroid-associated ophthalmopathy and dermopathy.
He was treated with radioactive iodine ablation. Photographs taken 1 year after treatment showed proptosis (Panel A) and pretibial myxedema (Panel B). Shortly thereafter he underwent orbital decompression in both eyes. At the time of the current presentation, his physical examination showed progression of the dermopathy, which was functionally limiting and resembled elephantiasis (Panel C). In addition, his hands were enlarged and coarsened, and his fingers had a clublike shape (Panel D).
Radiography of the hand showed periostitis of multiple phalangeal and metacarpal bones (Panel E, arrowheads), with diffuse swelling of the soft tissue, changes that were consistent with thyroid acropachy, a rare manifestation of Gravesβ disease.
Laboratory results showed that levels of thyrotropin-receptor antibodies were in excess of 40 IU per liter (normal range, β€1.75 IU per liter); the test did not allow for more precise measurement.
The patient was started on a combination treatment with intravenous immune globulin and rituximab. which appeared to halt the progression of his condition. At follow-up several months later there was no disease progression.
https://www.nejm.org/doi/full/10.1056/NEJMicm1506674
A 56-year-old man was referred to a dermatologist for assessment of the progression of his thyroid dermopathy. Three years earlier he had received a diagnosis of Gravesβ disease with thyroid-associated ophthalmopathy and dermopathy.
He was treated with radioactive iodine ablation. Photographs taken 1 year after treatment showed proptosis (Panel A) and pretibial myxedema (Panel B). Shortly thereafter he underwent orbital decompression in both eyes. At the time of the current presentation, his physical examination showed progression of the dermopathy, which was functionally limiting and resembled elephantiasis (Panel C). In addition, his hands were enlarged and coarsened, and his fingers had a clublike shape (Panel D).
Radiography of the hand showed periostitis of multiple phalangeal and metacarpal bones (Panel E, arrowheads), with diffuse swelling of the soft tissue, changes that were consistent with thyroid acropachy, a rare manifestation of Gravesβ disease.
Laboratory results showed that levels of thyrotropin-receptor antibodies were in excess of 40 IU per liter (normal range, β€1.75 IU per liter); the test did not allow for more precise measurement.
The patient was started on a combination treatment with intravenous immune globulin and rituximab. which appeared to halt the progression of his condition. At follow-up several months later there was no disease progression.
https://www.nejm.org/doi/full/10.1056/NEJMicm1506674
The New England Journal of Medicine
Thyroid Ophthalmopathy, Dermopathy, and Acropachy | NEJM
A 56-year-old man was referred to a dermatologist for assessment of the progression
of his thyroid dermopathy. Three years earlier, he had received a diagnosis of Gravesβ
disease with thyroid-assoc...
of his thyroid dermopathy. Three years earlier, he had received a diagnosis of Gravesβ
disease with thyroid-assoc...