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Graves’s disease

EPIDEMIOLOGY
Graves’ disease account  for 60- 80% of thyrotoxicosis. The prevalence varies among populations, reflecting genetic factors and iodine intake ( hight iodine intake is associated with an increased prevalence of Graves’s disease). Graves’ disease occurs in up to 2% of women but is one-tenth in frequent in men. The disorder rarely begins before adolescence and typically occurs between 20 and 50 years of age; it also occurs in the elderly.
CLINICAL MANIFESTATIONS
Signs and symptoms include features that are common to any cause of thyrotoxicosis as well as those specific for Graves’ disease. The clinical presentation depends on the severity of thyrotoxicosis, the duration of disease, individual susceptibility to excess thyroid hormone, and the patient’s age . In the elderly, features of thyrotoxicosis may be subtle or masked, and patients may present mainly with fatigue and weight loss, a condition know as apathetic thyrotoxicosis
Symptoms:

  1. hyperactivity, irritability, dysphoria (is a state of feeling unwell or unhappy; a feeling of emotional and mental discomfort as a symptom of discontentment, restlessness, dissatisfaction, malaise, depression, anxiety or indifference.)
  2. heat intolerance and sweating
  3. palpitations
  4. Fatigue and weakness
  5. Weight loss with increased appetite
  6. Diarrhea
  7. Polyuria
  8. Oligomenorrhea, loss of libido

Signs:

  1. Tachycardia, atrial fibrillation in the elderly
  2. Tremor
  3. Goiter
  4. Warm, moist skin
  5. Muscle weakness, proximal myopathy (Proximal muscle wasting and weakness is easily demonstratable.)
  6. Lid retraction or lag
  7. Gynecomastia

Excludes the signs of oththalmopathy and dermopathy specific for Graves’s disease.

LABORATORY EVALUATION
DIFFERENTIAL DIAGNOSIS

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Diagnosis approach to abdominal pain

HISTORY
Patients should first be asked about the time course of pain, both as past of the evaluation for a surgical abdomen and because once a surgical abdomen has been excluded the remainder of the evaluation will be guided by the chronicity of the symptoms along with the location pain.
The history should include:
– Location of pain
– Radiation of pain
– Factors that exacerbate or improve symptoms sush as food, antacids, exertion, defecation
– Associated symptoms including fevers, chills, weight loss or gain, nausea, vomiting, diarrhea, constipation, hematochezia, melena, jaudice, change of the color of urine or stool, change in the diameter of stool
– Past medical and surgical history, include rick factors for cardiovascular disease and details of previous abdominal surgeries
– Family history of bowel disorders
– Alcohol intake
– Intake of medications including over the counter medications sush as acetaminophen ( paracetamol), aspirin, and NSAIDs
– Menstrual and contraceptive history in women

PHYSICAL EXAMINATION
Physical examination will vary depending upon the location and chronicity of the patient’s symptoms. However, typical examination will be include:

  • Measurement of blood pressure, pulse and tempertature
  • Examination of the eyes and skin of jaundice
  • Auscultation and percussion of the chest
  • Auscultation of the abdomen for bowel sounds
  • Palpation of the abdomen for masses, tenderness, and peritoneal signs
  • Rectal examination including testing of stool for occutl blood
  • Pelvic examination in women with lower abdominal pain

ACUTE VERSUS CHRONIC PAIN
while an arbitrary interval, sush as 12 weeks, can be used to seperate acute from chronic abdominal pain, there is not strict time period that will classify the differential diagnosis unfaillingly. A clinic judgment must be made that considers whether this is an accelerating  process, one that has reached a plateau, or one that is longstanding but intermittent:

  • Pain of less than a fews days duration that has worsened progressively until the time of presentation is clearly acute
  • Pain that has remained unchanged for months or years can be safely classified as chronic
  • Pain that does not clearly fit either category might be called subacute and requires consideration of the differential diagnosis for both acute and chronic pain

Pain in a sick or unstable patient should generally be managed as acute, since patients with chronic abdominal pain may present with an acute exacerbation of a chronic problem or a new  and unrelated problem

ACUTE ABDOMINAL PAIN
Surgical abdomen- The first diagnoses that must be considered in patients with acute abdominal pain are those that may require urgent surgical intervention. The ” surgical abdomen” can be usefull defined as a condition with rapidly worsening prognosis in the absence of surgical intervention. Two syndromes that consititute urgent surgical referrals are obstruction and peritonitis. The latter encompasses most severe abdominal pathology since intraperitoneal hemorrhage or viscus performation typically present with common features of peritotitis.
Patients with acute surgical abdomens will often have a rapid symptom evolution, but patients who have evolved from partial to complete bowel obstruction, and it can be associated with unstable vital signs, fever, and dehydration.
Location and evolution of symptoms are helpful in narrowing the differential diagnosis, as in the classic evolution from visceral and periumbilical pain, to sharp right lower quadrant pain, in acute appendititis. a particularly high level of suspicion should be maintained for severe pathology in immunosuppressed patients and the elderly, where classic signs of peritoneal inflammation may be attenuated.
only after the clinician as satisfied that the abdominal presentation is not an acute surgical emergency can consideration of other diagnostic possibilities begin. Patients should not eat or drink while a diagnosis  of a surgical abdomen remains under consideration.

  1. Obstruction– Obstruction generally presents as pain together with anorexia, bloating, nausea, vomitting, and obstipation. Physical examination may reveal distention and high-pitched or absent bowel sounds. Abdominal percussion reveals tympany from proximally dilated loops of bowel. An abdominal mass, if present, may suggest anetiology for the obstruction.
  2. Peritonitis– Patients with peritonitis of any cause tend to ” look sick” and lie still minimize their discomfort. They may receive little benefit from analgasics. Althought rebound tenderness and its variants are classically thought to reflect peritonitis, abdominal wall rigidity and tenderness elicitable by percussion or very light palpation are also often overlooked features consistent with  a surgical abdomen . Others subtle signs of peritonitis that can be pursued include diminished bowel sounds and pain worsened when an examiner lightly bumps the stretcher.
  3. Initial diagnosis testing- Patients with a surgical abdomen should have the following laboratory measurements:
  • Complete blood count with differential
  • Electrolytes, BUN, Creatinin, and glucose
  • Aminotransferase, alkaline phosphase, and bilirubin
  • Lipase
  • Urinalysis
  • Pregnacy test in women of childearing potential

In the presence of fever or unstable vital signs, blood and urine clutures should be performed.
While these laboratory tests are important , they are not sufficient to rule in or rule out a diagnosis of surgical abdomen, as a surgical abdomen is clinical diagnosis.
Abdominal radiographs are a crucial step in decision making for the suspected surgical abdomen, as proximally dilated loops of bowel are the hallmark of intestinal obstruction, are free intraperitoneal air can confirm a suspicion of hollow organ perforation. Peritonitis is the absence of perforation or obstruction may not yeild any conclusive radiographic findings. Where CT scanning is immediately availble and necessary for further evaluation, as describerd below, abdominal plain films are not necessery, as they do not  provide additional information.

  1. Subsequent diagnostic testing –

Right upper quadrant pain- Pain involving the liver  or biliary tree is generally located in the right upper quadrant, but it may radiate to the back or epigastrium. Because hepatic pain only results when the capsule ( Glisson) of the liver is ” stretchesd “, most pain in the right upper quadrant is related to the biliary tree. Viral  or drug-included hepatitis can sometimes cause  acute right upper quadrant pain as well.
Initial assessment of patients  with right upper quadrant pain must consider serious causes and complications:

  • The presence of the fever and jaundice  in a patient with right upper quadrant pain leads to a clinical diagnosis of ascending cholangitis
  • Acute cholecystitis can also present as a systemically unwell patient with low-grade fever
  • Nonabdominal etiologies of upper abdominal pain must be considered

Once these possibilities have been cosidered, the history can be explored in more detail. Since gallstones are sush as a common cause of relatively benign pain, as well as the serious complications mentioned above, the history for right upper quadrant pain focuses initially on rick factors or gallstone disease and previous episodes of simila pain.

Epigastric pain- Epigastric pain that is relatively sudden in onset is suggestive of pancreatitis, particularly when it radiates to the back and is associated with nausea, vomitting, and anorexia

  1. Nonabdominal etiologies of upper abdominal pain
  2. Diagnostic testing for pancreatitis
  3. Diagnistic testing for dyspepsia

Lower abdominal pain

  1. nonabdominal etiologies of lower abdominal pain
  2. Diagnostic testing

Lower abdominal pain in  women
Generalized abdominal pain

  1. Diagnostic testing

CHRONIC  ABDOMINAL PAIN

  1. Initial diagnostic testing
  2. Subsequent diagnostic testing

Diagnosis approach to chest pain in adults

English: Pneumothorax in a young man with ches...

English: Pneumothorax in a young man with chest pain. Notice the air-fluid-level in the lateral left recessus. Deutsch: Spontanpneumothorax bei einem jungen Mann mit plötzlichem Thoraxschmerz. Beachte den Flüssigkeits-Luft-Spiegel im linken lateralen Rezessus. (Photo credit: Wikipedia)

This is a practice guideline. The components of this algorithm are evidence based wherever possible, but the sum of its parts has not been validated by any clinical studies.
DIAGNOSTIC ALGORITHM- The initial step prior to following the algorithm below is to perform a focused history and physical examination, and consider performing an ECG and or chest X-ray. Once a life- threatening etiology has been excluded, attempts should be make to identify the specific cause of symptoms and begin treatment

  • Step 1: Evaluate need for emergent care: Consider potentially life-threatening causes of chest pain. Patients it whom an ACS ( acute coronary syndrome: acute myocardial infraction or unstable angina) is suspected should receive emergent care ( chewing an aspirin).
    Emergent care should also be provided to patients who appear to be seriously ill and to patients in whom there is a suspicion a critical noncoronary diagnosis such as pulmonary ambolus, pneumothorax, aortic dissection, esophageal rupture or acute abdomen. For the patients who do not require emergent care , proceed to step 2.
  • Step 2: Emergent care not needed. In patients in whom a diagnosis  of stable CHD ( coronary heart disease or coronary artery disease) appears likely based on symptoms that are suggestive of angina and/or a history of cardiac rick factor, proceed to step 3, otherwise , proceed to step 5.
  • Step 3: Symptoms consistent with stable angina: Evaluate the patient for CHD, and consider staring outpatient managerment (therapy may be include aspirin, beta-blocker, nitroglycerin, and education about need for emergency care ) or admitting the patient to the hospital , especially if symptoms are progressive. It there is a concerm for angina secondary to valvular heart disease (eg, critical aortic stenosis), perform an echocardiogram prior to stress testing. Consider other cause of anginal chest pain , such as cardiac syndrome X and pulmonary hypertension. If the results of the evaluation do not demonstrate CHD, proceed to step 4, overwise, proceed to step 8.
  • Step 4: Evaluation for CHD was negative: Evaluate the patient for gastrointestinal disease. This evaluation may initially involve a trial of acid suppression. If there is no diagnosis and symptoms persist, proceed to step 6, overwise , proceed to step 8
  • Step 5:  Symptoms not sugestives of angina
  • Step 5a:For patients who are felt not to have an ischemic etiology for chest pain but who have significant rick factor for CHD, stress testing , while proceeding to step 5b
  • Step 5b: If symptoms suggest a musculosketetal etiology , a trial of an NSAID is appropriate, overwise, proceed to step 5c. If the pain persists, consider rib films, a bone scan, and plain or CT chest radiography. If there is no diagnosis and symptoms persist , proceed to step 6. otherwise, proceed to step 8
  • Step 5d: If symptom suggest a psychogenic etiology, evaluate the patient for a psychosocial soure of chest pain, overwise, proceed to step 5e. Diagnosis strategies may be include a therapeutic trial of an antidepressant medication of a psychiatric referral. If there is not diagnosis and symptoms persist , proceed to step 6. overwise proceed to step 8.
  • Step 5e: Consider chest anatomy as a guide to other less common causes of non-life-threatening chest pain including; chest wall pain ( eg, zorter, breast disease) ; other cardiac pain such as pericarditis; pathology of lung parenchyma, vasculature , or pleura, and pain refferred to chest from the gallbladdder , diaphragm, or from  a disc  herniation.
  • Step 6: Persistent chest pain: If the pain persists and evaluation for CHD ( as in  step 5a), musculasketetal pain ( as in step 5b), gastrointestinal pain ( as in step 5c) , psychogenic pain ( in step 5d) , and other causes ( as in step 5e) have not all been performed , those evaluations should now be undertaken.
    If there is no diagnosis and symptoms persist, proceed to step 7, otherwise , proceed to step 8
  • Step 7: Diagnosis evaluations negative: patient likely has chronic idiopathic chest pain. Since this is know to cause significant disability, consider referral to pain management center or medical symptom reduction program. No futher evaluation is required unless the patient has a change in symptoms or the symptoms are disabling .
  • Step 8: Cause of chest pain diagnosed: Proceed with therapy or additional evaluation as appropriate for the diagnosed condition.

COMMON PATIENT PRESENTATIONS

  1. Chest pain
  2. Abdominal pain
  3. Headache
  4. Back and Neck pain
  5. Fever, hyperthermia, chills and rash
  6. Pain and swelling of joints
  7. Syncope ( is defined  as a transient, sefl-limited loss of consciousness with an inability to maintain postural tone that is followed by spontaneous recovery. This definition excludes seizures, coma, shock, or other states of altered consciousness. Although most causes of syncope are benign, this symptom presages a life-threatening event in a small subset of patients.)
  8. Dizziness and Vertigo
  9. Acute visual loss and double vision
  10. Weakness and Paralysis
  11. Tremor and movement disorders
  12. Aphasias and related disorders
  13. Sleep disorders
  14. Dyspnea ( repiratory distress)
  15. Cough and hemoptysis
  16. Cyanosis
  17. Edema
  18. Nausea, vomiting and indigestion ( Indigestion (dyspepsia) is a vague feeling of discomfort in the upper belly or abdomen during or right after eating.)
  19. Weight loss
  20. Dysphagia
  21. Diarrhea ( is the condition of having three or more loose or liquid bowel movements per day-wiki), constipation, and malabsorption
  22. Gastrointestinal bleeding
  23. Jaudice and evaluation of liver function
  24. Ascites ( as hydroperitoneum)
  25. Azotemia ( hight levels of nitrogen- containing compounds, sush as urea, creatinine, various body waste compounds and other nitrogen-rich compounds in the blood) and urinary abnormalities
  26. Anemia and polycythemia
  27. Lymphadenopathy and slentomegaly
  28. Generalized fatigue

NERVOUS SYSTEM EXAMINATION

  1. General boservation
  2. Neck
  3. Face
  4. Speech and langauage
  5. Higher cerebral function
  6. Cranial nervers
  7. Motor function
  8. Co-ordination
  9. Sensory function

Babinski response & Hoffmann’s sign

DESCRIPTION
The Babiski response, or upgoing plantar response, is an abnormal cutaneous reflex response of the foot associated with upper moter neuron dysfunction. In a positive Babiski response, scratching the lateral plantar surface of the patient’s foot causes contraction of the extensor hallucis longus muscle and extension of the great toe ( normally the toe goes down)
CONDITION/S ASSOCIATED WITH
common
– cerebral infraction
– cerebral heamorrhage
– spinal cord injury
less common
– lacunar infarction, posterior limb internal capsule
– multiple sclerosis
– mass lesion ( tumour, abscess, AVM)
MECHANISM
Before 1 or 2 years of age, a noxious stimulus applied to the lower extremities cause involuntary ankle and foot dorsiflexion. The so-called ” flexion response” is a primitive reflex that disappears later in life. After 1 or 2 years of age, normal development of the central nervous system diminishes the flexion response, and the toes subsequently move downward. In a positive Babiski response, upper motor neuron dysfuction disrupts the normal plantar cutaneous reflex and the “flexion respinse” re-emerges. Upper motor neuron signs may coexist (e.g: spasticity, weakness, hyperreflexia). In the hyperacute period following upper motor neuron dysfunction, the Babiski response ( as with spasticity and hyperreflexia) may be absent, as it may take hours or days for these signs to emerge.
SIGN VALUE
The Babiski sign is an upper motor neuron sign. It may be absent initially in the hyperacute period following upper motor neuron dysfunction. Sensitivity: 45%, speccificity: 98%, Positive LR 19.0, Negative LR: 0.6
(McGee S, Evidence Based Physical Diagnosis, 2nd edition)
Note: In infant, Babinski positive in a healthy newborn
Hoffmann’s reflex: The test involves tapping the nail or flicking the terminal phalanx of the middle or ring. The positive response in seem with flexion of the terminal phalanx of the thumb.

Groin ( inguinal region)

English: Top view of inguinal hernia. Area sha...

English: Top view of inguinal hernia. Area shaved prior to hospitalisation and surgical repair procedure. Patient Michael C. (Photo credit: Wikipedia)

The groin ( inguinal region) is the area of junction between the anterior abdominal wall and thigh. In this area, the abdominal wall is weakened from changes that occur during development and a peritoneal sac or diverticulum, with or without abdominal contents, can therefore protrude through it, creating an inguinal hernia. This type off hernia can occur in both sexes, but it is most common in males.
The inherent wweakness in the anterior abdominal wall in the groin iss caused by changes that occur during the development off the gonads. Before the desscent off the testis and ovaries from their initial position high in the posterior abdominal wwall, a peritoneal outpouching ( the processus vaginalis) forms, protruding through the various layers off the anterior abdominal wall and acquirings from aech:
– transversalis forms its deepest covering:
– the second covering is formed by the musculature off the internal obique (, note: a covering from the transversus abdominis iss not acquired because the processus vaginalis passes under the arching fibers of this abdominal wall muscle):
– its most superficial covering is the aponeurosis of the external oblique.
As a result the processus vaginalis is transformed into a tubular structure with multiple coverings from the layers off the anterior abdominal wall. This forms the basic structure of the inguinal canal.
The final event in this development iss the descent of the testes into the scrotum or of the ovaries into the pelvic cavity. This process depends on the development of the gubernaculum (are embryonic structures which begin as undifferentiated mesenchyme attaching to the caudal end of the gonads (testis in males and overies in females).)
The development sequence in concluded in both sexes when the processus vaginalis obliterates ( block). If this does not occur or is incomplete, a potential weakness exists in the anterior abdominal wwall and an inguinal heria may development. In males , only proximal regions of the tunica vaginalis obliterate. The distal end expands to enclose mosst of the testis in the scrotum. In other words, the cavity of the tunica vaginalis in men forms as an extension of the developing peritoneal cavity that becomes separeted off during development.
Inguinal canal

The spermatic cord in the inguinal canal.

The spermatic cord in the inguinal canal. (Photo credit: Wikipedia)

The inguinal canal is a slit-like passage that extends in a downward and medial direction, just above and parallel to the lover haft of the inguinal ligament. It begins at the deep inguinal ring and continues for approximately 4cm, ending at superficial inguinal ring. The contents of the canal are the genital branch of the genitofemoral never, the spermatic cord in men and the round ligament of the uterus in women. Additionally, in both sexes, the ilio-inguinal nerve passes through part of the canal, exiting through the superficial inguinal ring with the other contents.
Deep inguinal ring
The deep ( internal) inguinal ring is the begining of the inguinal canal and is at a point midway between the anterior superior iliac spine and the pudlic symphysis. It is just above the inguinal ligament and immediately lateral to the inferoir epigastric vessels. Although sometimes referred to as a defect or opening in the transversalis fascia, it is actually the begining of the tubuar evagination of transversalis fascia that forms one of the coverings of the spermatic cord in men or the round ligament of the uterus in women.
Superficial inguinal ring ( external inguinal ring)

The suprergicial inguinal ring is  the end of the inguinal canal and is superior to the pubic tubercle. It is a triangular opening in the aponeurosis of the external obique,, with its apex pointing superolaterally and its base formed by the pubic crest. The two remaining sides of the triangle ( the medial crus and the lateral crus) are attached to the pubic symphysis and the pubic tubercle, respectively. At the apex of the triangle the two crura are held together by crossing ( intercrural ) fibers which prevent further widening of the superficial ring.
As with the deep inguinal ring, the superficial inguinal ring is actually the begining of the tubular evagination of the aponeurosis of the external oblique onto the structure traversing the inguinal canal and emerging from the superficial inguinai ring. This continuation of tissue over the spermatic cord is the external spermatic fascia
Anterior wall ( of the inguinal canal)
The anterior wall of the inguinal canal is formed along its entire legnth by the aponeusosis of the external oblique muscle. It is also reinforced laterally by the lover fibers of the internal oblique that  originate from the lateral two-thirds of the inguinal ligament. This adds an additional covering over the deep inguinal ring, which is a potential point of weakness in the anterior abdominal wall. Futhermore, as the internal oblique muscle covers the deep inguinal ring, it also contributes a layer ( the cremasteric fascia containing the cremasterng muscle) to the coverings of the structures traversing the inguinal canal
Posterior wall ( of the inguinal canal)
The posterior wall of the inguinal canal is formed along its entire length by the transversalis fascia. It is reinfored along its medial one-third by the conjoint tendon ( inguinal falx). The tendon is the combined insertion of the transversus abdominis and internal oblique muscles into the pubic crest and pectineal line
As with the internal oblique muscle’s reinforcement of the area of the deep inguinal ring, the position of the conjoint tendong posterior to the superficial inguinal ring provides additional support to the potential point of weakness in the anterior abdominal wall.

The relations of the femoral and abdominal ing...

The relations of the femoral and abdominal inguinal rings, seen from within the abdomen. Right side. (Photo credit: Wikipedia)

Roof ( superior wall)
The roof of the inguinal canal is formed by the medial one-half of the inguinal ligament. This rolled-under, free margin of the lowest part of the aponeurosis of the external obique forms a gutter or trough on which the contents of the inguinal cannal are positioned. The lacunar ligament reinforces most of the medial part of the gutter.